Atherosclerosis is a chronic inflammatory disease
characterized by endothelial dysfunction, lipid accumulation and
plaque formation within arterial walls, notably contributing to
cardiovascular morbidity and mortality on a global scale (1). According to the 2024 Heart Disease
and Stroke Statistics Update of American Heart Association,
cardiovascular diseases, for which atherosclerosis is the
underlying pathology in most cases, remain the leading cause of
death globally (2). Traditional
therapeutic approaches, such as the use of statins, have proven
effective in reducing cholesterol levels and decreasing the
incidence of cardiovascular events (3). However, these treatments are
frequently associated with adverse effects and may not be suitable
for all patients. Consequently, there is an urgent demand for
alternative therapeutic strategies that can effectively manage
atherosclerosis while minimizing side effects. Recent advancements
in nanotechnology have highlighted the potential of nanomaterials
to carry out a pivotal role in the treatment and prevention of
atherosclerosis (4).
Nanomaterials exhibit unique properties, including high surface
area, modifiability and targeted delivery capabilities, rendering
them particularly advantageous for drug delivery and the modulation
of cellular functions. Furthermore, exercise has been shown to
improve vascular function through various mechanisms, including
enhanced endothelial nitric oxide (NO) production and reduced
oxidative stress (5,6). Combining the therapeutic potential
of nanomaterials with the beneficial effects of exercise presents a
novel approach to enhance vascular health and combat
atherosclerosis.
Previous research suggests that nanomaterials can
modulate the inflammatory response in vascular cells, thereby
mitigating the progression of atherosclerosis (7-9).
Certain nanoparticles, for example, have been shown to suppress the
expression of pro-inflammatory cytokines and facilitate the
resolution of inflammation in endothelial cells (ECs) (9,10). Nanomaterials can potentially halt
or reverse atherosclerosis by targeting inflammatory pathways
(11). Combining these with
exercise, which releases factors such as NO to improve endothelial
function (12), may enhance
their therapeutic effects (13).
Exercise could also increase the delivery and effectiveness of
nanomaterial treatments in the vascular system.
Previous research has highlighted the importance of
understanding the interactions between nanomaterials and the
vascular microenvironment (14,15). The distinctive properties of
nanomaterials considerably affect their behavior within biological
systems, encompassing aspects such as biocompatibility,
biodistribution and pharmacokinetics (16). Consequently, an in-depth
examination of these interactions is imperative for optimizing the
design of nanomaterials specifically engineered for vascular
applications.
The present review explores how combining
nanomaterials with physical exercise can impact atherosclerosis. It
examines numerous studies on using nanomaterials to improve
endothelial function, reduce inflammation and aid lipid clearance
in atherosclerotic lesions. Additionally, it examines how exercise
enhances the effectiveness of nanomaterial therapies and the
biological mechanisms involved. Ultimately, integrating
nanomaterials with physical exercise presents a promising strategy
for improved vascular health and reduced cardiovascular disease
burden. Future research should focus on understanding these
synergistic effects and exploring clinical applications for
managing atherosclerosis.
Nanomaterials have emerged as promising agents for
the protection of vascular ECs by reducing oxidative stress and
inflammation, and enhance the release of NO (17,18). For example, gold nanoparticles
have been demonstrated to activate the nuclear factor erythroid
2-related factor 2 signaling pathway (19), which reduces reactive oxygen
species (ROS) production. This activation markedly reduces
oxidative stress in ECs, preserving their function and integrity
(19). Moreover, silica
nanoparticles carrying anti-inflammatory drugs effectively inhibit
the NF-κB pathway, reducing endothelial inflammation (20). This is key as chronic
inflammation carries out a key role in endothelial dysfunction and
the advancement of atherosclerosis (20). Additionally, carbon-based
nanomaterials can mimic endothelial nitric oxide synthase (eNOS)
activity, promoting the release of NO, which is key for
vasodilation (21). This
increase in NO improves vascular tone and contributes to the
protective effects on ECs, highlighting their potential as
treatments for vascular diseases.
Nanomaterials carry out a key role in influencing
VSMC phenotypes by inhibiting pathological proliferation and
maintaining a contractile phenotype (22). Polymer-based nanoparticles are
used to deliver miR-145, which regulates the transcription factor
Krüppel-like factor (KLF) 4, key for VSMC phenotype modulation
(23). By modulating the
expression of KLF4, these nanoparticles effectively inhibit the
pathological VSMCs proliferation, a key characteristic of
atherosclerosis (24,25). Furthermore, magnetic
nanoparticles activate the RhoA/ROCK pathway, thereby promoting the
maintenance of a contractile phenotype in VSMCs. This mechanical
activation is essential for preventing the phenotypic transition
from a contractile to a synthetic state, a process frequently
associated with vascular remodeling and the development of
atherosclerotic plaques (26).
Additionally, nanofibrous scaffolds provide mechanical cues that
influence the remodeling of the extracellular matrix, consequently
affecting collagen secretion and the overall vascular architecture
(27).
Optimization of nanomaterial-based targeted delivery
systems is essential for improving their therapeutic efficacy in
vascular applications. Surface modification techniques, such as
polyethylene glycol-ylation, have been utilized to extend the
circulation time of nanoparticles within the bloodstream (28), thereby enhancing their
bioavailability and reducing premature clearance by the immune
system. Moreover, the incorporation of targeting ligands, such as
RGD peptides, can substantially increase the specificity of these
nanomaterials for diseased vascular sites, facilitating more
effective treatment of conditions such as atherosclerosis (29). Stimuli-responsive systems such as
pH-sensitive nanocarriers allow localized drug release in the
acidic environments of atherosclerotic plaques, increasing drug
efficacy and reducing side effects (30). Combining therapies, such as
photothermal treatment with drug delivery, enables precise control
over treatment timing and location, optimizing outcomes in vascular
diseases (31). These strategies
enhance the role of nanomaterials in vascular health therapy.
Exercise applies mechanical forces to the vascular
endothelium, mainly through blood flow-induced shear stress, which
activates signaling pathways key for endothelial function (32). This includes the activation of
eNOS, leading to increased NO production, essential for vascular
relaxation and homeostasis (33). Shear stress also boosts KLF2
expression, protecting ECs by regulating inflammation and vascular
tone (34). Additionally,
exercise-induced blood flow influences the cell cycle of vascular
wall cells, promoting their proliferation and migration, key for
vascular remodeling and repair (35). Shear stress activates
mechanotransduction pathways, such as the integrin-FAK-Akt
signaling cascade, which are important for ECs to adapt to
mechanical stimuli and preserve vascular integrity (36,37).
Physical exercise triggers metabolic changes in
various tissues, including the vascular system, by activating AMPK
and Peroxisome proliferator-activated receptor γ coactivator 1-α
(PGC-1α), which increase mitochondrial function and biogenesis
(38,39). This enhances energy production
and oxidative capacity in ECs, improving vascular function.
Exercise also facilitates lipid metabolism by delivering liver X
receptor agonists through nanocarriers, regulating cholesterol and
inflammation in vascular tissues (40,41). Increased autophagic flux,
supported by exercise and mTOR-inhibiting nanomedicines (42), helps degrade damaged organelles
and proteins (43,44), enhancing cellular health and
vascular healing.
Physical exercise triggers changes in the vascular
microenvironment, affecting circulating factors that improve
vascular function (45). A key
element is irisin, a myokine released during exercise, which
increases vascular permeability and aids drug delivery, especially
in nanomedicine. Moreover, exercise also redistributes immune
cells, notably stabilizing atherosclerotic plaques through the
activation of Ly6C^low monocytes (46). This alteration in immune cell
dynamics carries out a key role in promoting vascular health and
stability. Additionally, exercise-regulated sympathetic nervous
system activity can enhance the distribution and effectiveness of
therapeutic agents, including nanomedicines, in targeted vascular
tissues (47). These adaptations
underscore the role of exercise in improving vascular health and
function.
Exercise and nanomaterials work together at the
molecular level to combat atherosclerosis through several
mechanisms (51). A key
mechanism is epigenetic regulation, where exercise boosts the
demethylation effects of histone deacetylase inhibitors delivered
by nanocarriers, enhancing their therapeutic impact on vascular
health (52,53). Additionally, exercise-induced
exosomes and exosome-like nanoparticles interact to strengthen
cellular signaling pathways vital for cardiovascular disease
prevention and treatment (54).
Furthermore, the timing of exercise can affect the efficacy of
pH-sensitive nanomedicines, indicating that exercise-related
biological rhythms can influence nanomaterial therapy outcomes
(55). These molecular insights
underscore the complex interplay between exercise and
nanotechnology in the treatment of atherosclerosis, emphasizing the
need for a tailored approach that considers both physical activity
and nanomaterial properties.
Advanced imaging technologies, such as cutting-edge
imaging technologies, have markedly validated the combined effects
of exercise and nanomaterials. PET/MRI has been key in tracking
nanoparticle distribution during exercise, offering insights into
treatment dynamics by visualizing their accumulation in
atherosclerotic lesions (56).
Furthermore, super-resolution microscopy has precisely observed
nanomedicine deposition on plaque fibrous caps after exercise,
suggesting enhanced targeted delivery (57). Additionally, Raman spectroscopy
effectively monitors biochemical changes in plaques post-exercise
and nanomaterial treatment (58,59). Collectively, these advanced
imaging techniques not only validate the synergistic effects
observed in preclinical models but also pave the way for future
clinical applications, highlighting the potential of integrating
exercise with nanomedicine to mitigate atherosclerosis.
Numerous therapeutic drugs can slow atherosclerosis
by enhancing SMC function. Several therapeutic agents include short
hairpin RNA, small interfering (si)RNAs, natural extracts and
chemicals (60-63). However, the application of these
therapeutic agents for the treatment of metabolic disorders is
unfortunately limited by pharmacological issues, including drug
instability, rapid degradation and poor specificity (64).
Nanomedicine has attracted widespread attention due
to its advantage in drug delivery (65). As theragnostic agents with high
molecular specificity, nanoparticles have been shown to serve as
drug delivery carriers to facilitate the diagnosis and treatment of
diseases. Due to their dimensions <100 nm (ASTM International,
2006), the advantages of nanoparticles include i) efficient
delivery of drug insoluble or poorly soluble in water, ii) targeted
drug delivery in a tissue/cell type -specific pattern, iii)
controlled absorption and sustained drug release, iv) delivery of
drugs to intracellular sites of action or to the soma, v) high
binding ability and capture efficiency due to a relatively high
surface to volume ratio, vi) delivery of two or more drugs for
combination therapy due to the nano-sizes, vii) visualization of
drug sites by combining therapeutic agents with imaging modalities;
viii) protect the therapeutic agents and increase their stability,
viiii) immune-evading and tumor-targeting capabilities and x) great
biocompatibility and high drug loading efficiency in vivo
drug efficacy (66-70). Nanomedicine has incomparable
advantages over ordinary drugs. It has high solubility, can greatly
enhance the absorption and bioavailability of oral drugs, can make
the drug pass through the blood-brain barrier to act on the central
nervous system, can penetrate the epidermis to enhance the
absorption of the preparation and can also enhance the drug
targeting. Therefore, nanoparticles have a wide application in the
field of biomedicine due to their aforementioned medical
characteristics.
Despite its advantages, nanomedicine has several
drawbacks, such as toxicity, genotoxicity and carcinogenicity.
Given their small size, nanoparticles can circulate in the body and
accumulate in tissues, posing health risks. Metal nanoparticles
such as titanium dioxide, gold, silver and platinum can harm human
health. For example, 21 nm titanium dioxide nanoparticles can cause
neuroinflammation, brain and spleen injury, heart damage, and lung
toxicity (71,72). Gold nanoparticles have been found
in urine and blood 3 months after exposure (73), and platinum nanoparticles
accumulate in the liver and spleen, causing liver and kidney
toxicity (74). To date, the
advantages of using nanoparticles over traditional medical
strategies seem to outweigh their disadvantages. Nanoparticles in
medicine must be designed carefully and validated through a series
of experiments to ensure their safety.
Nanomedicine, using nanomaterials such as
nanoparticles, is rapidly advancing in treating atherosclerosis
(Fig. 1). Nanotechnology
markedly impacts healthcare, including targeted nanotherapeutics
(75), medical imaging (76), diagnostics (77), vaccines (78) and regenerative medicine. Previous
studies show nanoparticles can slow vascular disease by targeting
vascular cells (79-110) (Table I). Due to its importance, several
reviews cover the role of nanomedicine in treating diseases such as
cancer, atherosclerosis and diabetes (77,111,112). Therefore, it is important to
increase awareness of the benefits of pharmaceutical nanotechnology
and existing treatments for atherosclerosis (Fig. 1).
Imbalanced SMC proliferation can cause pathological
angiogenesis, leading to plaque growth and rupture in coronary
arteries, potentially resulting in cardiovascular mortality.
Accurate ultrasound detection of nanoparticles on atherosclerotic
plaque neovascularization can aid in early diagnosis of unstable
plaques. Super-paramagnetic iron oxide particles (SPIONs)
conjugated with annexin A5 are more effective than non-targeted
SPIONs in identifying atherosclerotic lesions in rabbits (113). Additionally, synthetic high
density lipoprotein nanoparticles with Apo A1 (APOA1) and triphenyl
phosphonium cations can detect mitochondrial membrane potential
collapse and apoptotic cells (114). The mTOR pathway is involved in
VSMC and pulmonary arterial SMCs (PASMCs) proliferation in
pulmonary arterial hypertension (115,116), and administration of mTOR siRNA
nanomedicines can markedly inhibit PASMC proliferation after
hypoxia (115). Nanoparticles
notably attenuate oxidized low-density lipoprotein-induced SMC
proliferation and thrombosis through downregulating the expression
of scavenger receptor and key proinflammatory markers, implying the
promise of nanomedicine for next-generation cardiovascular
therapeutics (117). Therefore,
nanomedicines carrying drugs may be promising therapeutics for
diseases associated with the proliferation of SMCs (Fig. 2).
Nanomedicine offers an effective approach to
treating atherosclerosis by improving SMC dysfunction and
inhibiting cell proliferation (118). In early atherosclerosis, SMCs
increase adhesion molecules and pro-inflammatory cytokines. A
nano-delivery system, including 17-βE loaded nano-emulsions,
notably reduced the expression of these molecules (119), highlighting its therapeutic
potential. Additionally, miR-146a-5p nanomedicines, which target
inflammation via the NF-κB pathway, reduced neointimal hyperplasia
in rat arteries post-revascularization (120). Thus, nanomedicines can
effectively deliver drugs to injury sites, showing promise against
neointimal hyperplasia.
Atherosclerosis is a chronic disease marked by lipid
deposition and inflammation in arterial walls (121), leading to plaque growth and
potential rupture, which can cause myocardial infarction (MI). The
severity of the disease is influenced by plaque size and
composition, affecting stability. Unstable plaques may rupture
under altered blood flow, blocking capillaries and causing
cardiovascular events such as MI, stroke and peripheral artery
disease (122). Endothelial
injury exacerbates atherosclerosis by promoting platelet
aggregation, coagulation and SMC proliferation (123), making the endothelium vital in
plaque development, stability and rupture.
Previous studies indicate that nanoparticles can
deliver drugs to ECs for diagnosing or treating atherosclerotic
diseases (79-110,124,125) (Table I; Fig. 2). Ultrasound imaging of plaque
neovascularization can improve early detection of unstable plaques.
VEGFR-2 targeting antibody nano-microbubbles are more effective
than blank ones in detecting plaques in rats (126). IL-10, an inflammation
regulator, suppresses pro-inflammatory responses in atherosclerosis
by inhibiting NF-κB activation (127). Branched poly (β-amino ester)
nanoparticles with IL-10 plasmid DNA can slow atherosclerosis
progression (128). The
nanoparticle-VHPKQHRGGSGC peptide drug delivery system targets ECs,
enhancing the anti-inflammatory effects of IL-10 on atherosclerotic
plaques (128). Triptolide
could inhibit inflammatory responses and angiogenesis in ECs
(129), which might improve the
symptoms and delay the progression of atherosclerosis. APRPG
(Ala-Pro-Arg-Pro-Gly) peptide-modified nanoliposomes, a novel
sustained-release drug delivery system targeting ECs, enhances
inhibitory effects of triptolide on laser-induced
neovascularization (130).
Nanomedicine not only inhibits angiogenesis but also enhances
endothelial function to treat atherosclerosis. In primary ECs,
amorphous selenium quantum dots improved endothelium-dependent
relaxation and accelerated wound healing, reducing atherosclerotic
plaque in aortic arteries (131). Encapsulating cherry extract
from Prunus avium L. in nanoparticles protected HUVECs from
oxidative stress and decreased ROS production (132). Molybdenum disulfide
nanoparticles (MoS2 NPs) show promise as a multifunctional
therapeutic, reversing hydrogen peroxide-induced endothelial
senescence by enhancing autophagy (133). Additionally, mRNA-p5RHH
nanoparticles can be assembled into nuclease-resistant
nanoparticles (134).
Cyclin-dependent kinase inhibitor p27Kip1 nanoparticles
target endothelial denudation areas, promoting vessel
reendothelialization and reducing neointima formation after injury
(135). Mesoporous silica
nanoparticles with CD9 antibodies deliver rosuvastatin to senescent
ECs and macrophages, slowing atherosclerosis progression in
apoE−/− mice (136).
These EC-targeted nanotherapies are promising for atherosclerosis
and other cardiovascular diseases. For instance, silica-coated
magnetic iron oxide nanoparticles can label endothelial progenitor
cells (EPCs) from male rats, forming magnetized EPCs (137). Transplanting these EPCs
improves cardiac function, reduces infarction size and decreases
myocardial cell apoptosis, enhancing myocardial infarction
treatment (138).
Invasive therapy technology, such as NO-producing
vascular stents, offers a novel therapeutic strategy for treating
arterial stenosis. A study by Yang et al (139) demonstrated that stents
functionalized with 3,3-diselenodipropionic acid and
S-nitrosothiols implanted into vessels via nanomaterials can
produce NO, promote EC growth, reduce platelet activation and VSMC
activity (Fig. 2). This
nanocoating technique creates an endothelium-like environment,
presenting a novel treatment strategy for cardiovascular
diseases.
Atherosclerosis is an inflammatory disease of the
artery walls involving immune cells such as macrophages, which are
key in its progression (77,140). Targeting macrophage-related
processes offers potential for diagnostics and therapies. Early in
atherogenesis, arterial ECs recruit macrophages via
chemokine-receptor interactions and adhesion molecules such as
intercellular adhesion molecule 1 and vascular cell adhesion
molecule 1 (141). This
recruitment system is redundant, allowing for the inhibition of
plaque formation by targeting multiple adhesion molecules (141). Additionally, vascular
macrophages contribute to atherosclerosis through the expression of
the olfactory receptor Olfr2 and related signaling molecules
(142). Aberrant activation and
polarization of arterial macrophages affect apoptosis and
efferocytosis, associate with lipid accumulation and the
inflammatory response in macrophages to the development of
atherosclerotic lesions (143).
Indeed, suppression of macrophages reduced atherosclerosis in mice
(144), emphasizing the
importance of detecting subclinical disease in humans for
monocyte-directed treatment.
Nanotechnology could enhance atherosclerosis
treatment by developing new diagnostic and therapeutic methods to
lower cardiovascular disease risk. Gao et al (145) introduced a biomimetic drug
delivery system using ROS-responsive nanoparticles coated with
macrophage membranes, which block proinflammatory cytokines to
reduce inflammation. This approach, along with pharmacotherapy,
increases atherosclerosis treatment efficacy, indicating that
macrophage membrane-coated systems are well-suited for inflammatory
diseases (145).
Rapamycin-loaded nanoparticles using activated macrophage membrane
proteins have shown promise by inhibiting macrophage proliferation
and reducing inflammation and plaque changes (146). Long-term use of PLGA
nanoparticles enhances lysosomal degradation, reduces macrophage
apoptosis, necrotic core formation and cytotoxic protein
aggregates, while increasing fibrous cap formation (147), suggesting they can alleviate
macrophage lysosomal dysfunction in atherosclerosis. RNA
interference (RNAi) with nanoparticles effectively inhibited key
adhesion molecules, reducing macrophage recruitment to
atherosclerotic lesions (141).
Thus, nanomedicine can improve atherosclerosis by targeting
macrophages (Fig. 2). However,
nanoparticles can also worsen vascular disease; for example,
inhaled silica nanoparticles can exacerbate lesions and increase
pro-inflammatory M1 macrophages (148).
Exercise-induced acute and adaptive physiological
changes may notably improve the in vivo microenvironment for
nano-drugs, thereby enhancing their efficacy (149). This synergistic effect can be
attributed to several mechanistic pathways: i) Hemodynamics and
vascular permeability: Exercise increases cardiac output and tissue
blood flow, potentially facilitating the delivery and accumulation
of nanoparticles in target tissues such as the heart or skeletal
muscle, ii) metabolic and immune reprogramming: Exercise-induced
metabolic alterations, such as reduced insulin resistance and
immunomodulation, including an increase in anti-inflammatory M2
macrophages, may enhance the susceptibility of target cells to
therapeutic agents such as nucleic acids and small molecules, while
also mitigating inflammatory responses that could degrade
nanoparticles, iii) cellular uptake: The upregulation of specific
cell surface receptors, such as certain integrins, during exercise,
when aligned with the targeting ligands on nanoparticles, could
markedly enhance cellular internalization. Consequently, exercise
should not be viewed merely as an adjuvant therapy but rather as a
'bio-enhancer' that actively modulates the host environment to
optimize pharmacokinetics.
Despite promising advancements in preclinical
research and the application of nanomaterials, challenges remain
that could hinder progress. A primary challenge lies in the ethical
implications associated with ongoing clinical trials, especially
with fast-evolving science and issues such as COVID-19 (150). Ensuring the relevance and value
of clinical trials as new information emerges is key for
maintaining public trust and scientific integrity. Furthermore, the
integration of nanomaterials into clinical practice presents
notable obstacles, including concerns regarding toxicity,
immunogenicity and regulatory approval processes (151). However, these challenges also
present opportunities for innovation and interdisciplinary
collaboration. By fostering partnerships among researchers,
clinicians and regulatory bodies, the field can develop robust
frameworks that address these issues while advancing scientific
knowledge and improving patient outcomes. Future research should
focus on overcoming these barriers to fully harness the potential
of emerging technologies in personalized medicine and preclinical
research.
Nanoparticles have several advantages over
traditional therapeutic agents, including the ability to target
specific tissues or cells, controlled drug release and reduced
toxicity. Nonetheless, there are important limitations and
challenges in cardiovascular nanomedicine that should be noted
(79-110,152,153) (Table I). Future advancements in
nanoparticle-based therapies for the diagnosis and treatment of
arteriosclerosis are anticipated, with ongoing development and
refinement in this field (4,7,77). These nanoparticles have the
potential to inhibit pro-atherogenic processes in macrophages,
VSMCs and ECs, thereby enhancing the resolution of inflammation and
stabilizing plaques. Furthermore, this work addresses the enduring
challenge of translating nanomaterials into clinical applications
by summarizing current obstacles and suggesting avenues for
innovation and enhancement in nanomaterial design. This may involve
the creation of novel and more efficacious therapeutic agents, the
development of improved targeting strategies to ensure precise
delivery of nanoparticles to plaque sites, and the integration of
nanoparticle-based therapies with other treatment modalities, such
as surgical interventions or stenting.
The utilization of nanoparticles coated with natural
membranes derived from cells or extracellular vesicles for targeted
drug delivery to the skin has been explored (154). Recent advancements in imaging
techniques have enabled scientists to observe and comprehend the
interactions of nanoparticles with biological systems at an
ultrastructural level (155).
Techniques such as cryo-electron microscopy, super-resolution
microscopy and advanced spectroscopy are pivotal for elucidating
the safety, biodistribution, and fundamental mechanisms of action
of nanomedicines. Interfacial self-assembly nanoarrays pertain to
spontaneously organized nanostructures at interfaces, which depend
on the intrinsic properties of the materials involved, including
surface energy, molecular structure and interactions (156). Moreover, plasmonic alloys have
been shown to enhance metabolic fingerprints, facilitating the
rapid diagnosis and classification of MI (157). This advancement holds the
potential to reduce the duration of emergency department visits and
improve MI treatment outcomes. Thus, nanomedicine is transforming
from a simple 'drug deliveryman' to a 'comprehensive medical
platform' that can intelligently interact with life systems,
analyze diseases at the molecular level, and achieve precise
diagnosis and efficient treatment integration.
It is imperative to critically evaluate the
heterogeneous findings on nanomaterials. Some studies highlight
their benefits, while other studies raise concerns about their
biocompatibility and long-term implications (158,159). A balanced approach is needed to
weigh positive results against potential risks, guiding the
development of standardized clinical protocols. Future research
should prioritize elucidating the mechanisms that govern the
interactions between nanomaterials and cardiovascular cells,
alongside optimizing nanomaterial design for improved efficacy and
safety. There is an urgent need for rigorously designed clinical
trials to evaluate the long-term impacts of nanomaterials in the
treatment of atherosclerosis. Additionally, interdisciplinary
collaborations among materials scientists, biologists and
clinicians will be key to advancing this field.
The present review highlights the considerable
potential of the nano-platform for applications such as
tumor-targeted therapy; however, there are considerable challenges
associated with its clinical translation, particularly in relation
to long-term in vivo safety and biodistribution. Due to
their material composition and size, the nanoparticles are likely
to undergo sequestration and clearance predominantly in the liver
and spleen. The potential risks of long-term toxicity,
immunogenicity and off-target accumulation necessitate
comprehensive evaluation in future studies, particularly through
systematic long-term animal experiments. Addressing these safety
concerns is essential for the advancement of this platform toward
clinical application and will constitute a primary focus of
forthcoming research.
The present review posits a key perspective:
Nanomaterials and exercise should not be viewed as independent
interventions but rather as synergistic agents that converge on
common molecular pathways, thereby offering a transformative
approach to cardiovascular therapy. This integration propels the
field forward in two notable ways. Firstly, on a mechanistic level,
it introduces a novel concept of 'bidirectional regulation', for
example, in the context of inflammatory pathways, exercise promotes
an anti-inflammatory state by modulating myokines such as IL-6,
which increases IL-10 and decreases TNF-α levels (160). Concurrently, nanomaterials can
be engineered to deliver anti-inflammatory agents (161), such as siRNA targeting TNF-α,
directly to gut microbiota for ulcerative colitis therapy (162). This dual approach effectively
remodels the inflammatory microenvironment through both 'systemic
modulation' and 'localized precision strike' strategies. Secondly,
at a translational level, it introduces an innovative paradigm of
'preconditioning combined with therapy'. Exercise acts as a safe
and cost-effective systemic 'preconditioning' strategy that
optimizes the overall physiological environment by enhancing
vascular function and reducing oxidative stress (163). This creates a less favorable
environment for the subsequent administration of nanotherapeutics.
This integrated approach not only has the potential to enhance the
efficacy of monotherapies but also addresses the multi-pathway
dysregulation characteristic of complex diseases, representing a
key direction for the future integration of precision medicine and
lifestyle interventions.
Not applicable.
QZ, GLZ, WS and LHY conceived the structure of the
manuscript; QZ and LY drafted the initial manuscript; QZ, GZ, WS,
JC and LHY revised and edited the manuscript. All authors
contributed to the preparation of this manuscript. All the authors
approved the final manuscript. Data authentication not
applicable.
Not applicable.
Not applicable.
The authors declare that they have no competing
interests.
Not applicable.
No funding was received.
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