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Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review)

  • Authors:
    • Wen Pei
    • Ping Lu
    • Chenhuan Ding
    • Ying Li
    • Yong Li
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, P.R. China, Department of Cardiology, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, P.R. China, Department of Traditional Chinese Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, P.R. China, Department of Cardiology, Jing'an District Hospital of Traditional Chinese Medicine, Shanghai 200072, P.R. China
    Copyright: © Pei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 120
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    Published online on: March 12, 2026
       https://doi.org/10.3892/ijmm.2026.5791
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Abstract

Cardiovascular and cerebrovascular diseases (CCVDs) have become prominent global health threats, presenting substantial challenges due to their intricate pathological mechanisms and diverse clinical manifestations. Tanshinone IIA (TSA), an active compound derived from the traditional Chinese medicinal herb Salvia miltiorrhiza, exhibits notable therapeutic potential in these diseases due to its multifaceted mechanism of action. TSA protects the cardiovascular and cerebrovascular systems by inhibiting inflammation, reducing oxidative stress, preventing apoptosis and fibrosis, and modulating key signaling pathways, including toll‑like receptor 4/NF‑κB, PI3K/AKT and nuclear factor erythroid 2‑related factor 2/heme oxygenase‑1. Notably, considerable progress has been made in applying TSA to conditions such as atherosclerosis, myocardial infarction, heart failure and hypertension. The present review synthesizes current research on the molecular mechanisms of TSA in treating CCVDs and highlights innovations in nanodelivery systems (for example, rHDL, TPP‑TPGS/LPNs and CBSA‑PEG‑TSA‑NPs) that enhance its therapeutic efficacy by improving solubility, prolonging its half‑life and enhancing targeting capabilities. These advancements not only establish a foundation for the broader clinical application of TSA in CCVDs but also offer valuable insights for the development of new therapeutic agents.
View Figures

Figure 1

Major active components of Salvia
miltiorrhiza. The active components of Salvia miltiorrhiza can be
categorized into lipophilic and hydrophilic constituents. The
lipophilic components (tanshinones) include Tanshinone I,
Tanshinone IIA, Tanshinone IIB, Cryptotanshinone, Dihydrotanshinone
and Tanshinolactone. The hydrophilic components (phenolic acids)
comprise Salvianolic acid A, Salvianolic acid B and Salvianic acid
A.

Figure 2

Pharmacological activities and
functions of Tanshinone IIA. Tanshinone IIA exerts multiple
pharmacological effects through modulation of various molecular
pathways, including anti-inflammatory, antioxidant,
anti-mitochondrial apoptosis, antiallergic, antithrombotic,
antifibrotic, antitumor, immunomodulatory, vasodilatory (via
regulation of the RAS system) and neuroprotective activities. ACh,
acetylcholine; ADP, adenosine diphosphate; AKT, protein kinase B;
α-SMA, alpha-smooth muscle actin; AMPK, AMP activated protein
kinase; CAT, catalase; CHOP, CCAAT-enhancer-binding protein
homologous protein (C/EBP homologous protein); CDK4, cyclin,
dependent kinase 4; cGMP, cyclic guanosine monophosphate; COX2,
cyclooxygenase2; COL-1, collagen type 1; eNOS, endothelial nitric
oxide synthase; ERK, extracellular signal-regulated kinase; Gpx,
glutathione peroxidase; JNK, c-Jun N-terminal kinase; GPR78,
glucose-regulated protein 78; HO-1, heme oxygenase 1; Hsp90, heat
shock protein 90; IL-6, interleukin-6; LKB1, liver kinase B1; LTC4,
leukotriene C4; MDA, malondialdehyde; MyD88, myeloid
differentiation primary response gene 88; mTOR, mechanistic target
of rapamycin; NF-κB, nuclear factor kappa-light-chain-enhancer of
activated B cells; NLRP3, NLR family pyrin domain-containing 3;
NOX2, NADPH oxidase 2; Nrf2, nuclear factor erythroid 2-related
factor 2; PI3K, phosphatidylinositol 3 kinase; PGD2, prostaglandin
D2; PKC, protein kinase C; PKG, protein kinase G; PLCβ3,
phosphorylation of phospholipase cβ3; PP2A, protein phosphatase 2A;
PTEN, phosphatase and tensin homolog; PTPN, protein tyrosine
phosphatase non-receptor type; SHP, Src homology 2
domain-containing protein tyrosine phosphatase; SIRT1, sirtuin 1;
SOD, superoxide dismutase; TP53, tumor protein 53; TGF-β,
transforming growth factor-β; TLR4, toll like receptor 4; TNF-α,
tumor necrosis factor-alpha; TRPV4, transient receptor potential
vanilloid 4; TXA2, thromboxane A2; 6-OHDA,6-hydroxydopamine.

Figure 3

Role of Tanshinone IIA in the
development of cardiovascular and cerebrovascular diseases.
Tanshinone IIA demonstrates therapeutic efficacy against a wide
range of cardiovascular and cerebrovascular diseases, including
atherosclerosis, cardiac hypertrophy, myocardial infarction,
myocardial ischemia-reperfusion injury, cerebral
ischemia-reperfusion injury, heart failure, hypertension, cardiac
fibrosis, arrhythmia and stroke.

Figure 4

Molecular mechanisms of Tanshinone
IIA in the treatment of atherosclerosis and hypertension. AKT,
protein kinase B; APOB, apolipoprotein B; ATF3, activating
transcription factor 3; eNOS, endothelial nitric oxide synthase;
ET-1, endothelin 1; KLF4, Krüppel-like Factor 4; LOX-1, lectin-like
oxidized LDL receptor 1; MDA, malondialdehyde; MMP2, matrix
metalloproteinase 2; MTP, microsomal triglyceride transfer protein;
NO, nitric oxide; PDK1, pyruvate dehydrogenase Kinase 1; PI3K,
phosphatidylinositol 3 kinase; ROS, reactive oxygen species; SOD,
superoxide dismutase; STAT6, signal transducer and activator of
transcription 6; TIMP2, tissue inhibitor of metalloproteinases 2;
TNF-α, tumor necrosis factor-α; TSA, tanshinone IIA; ERK,
extracellular signal-regulated kinase; JNK, c-Jun N-terminal
kinase; NF-κB, nuclear factor κ-light-chain-enhancer of activated B
cells; IL-6, interleukin-6.

Figure 5

Molecular mechanisms of Tanshinone
IIA in the treatment of myocardial hypertrophy, myocardial
infarction, and heart failure. α-SMA, α-smooth muscle actin; AKT,
protein kinase B; ALKBH5, AlkB Homolog 5; ASC, Apoptosis-associated
speck-like protein containing a CARD; AMPK, AMP activated protein
kinase; ANP, atrial natriuretic peptide; BNP, brain natriuretic
peptide; COL-1, collagen type 1; Cys-C, cystatin c; IL-6,
interleukin-6; mTOR, mechanistic target of rapamycin; NF-κB,
nuclear factor kappa-light-chain-enhancer of activated B cells;
NLRP3, NLR family pyrin domain-containing 3; PDHK1, pyruvate
dehydrogenase kinase 1; PI3K, phosphatidylinositol 3 kinase; PKG,
protein kinase G; PTEN, phosphatase and tensin homolog; TLR4, toll
like receptor 4; TNF-α, tumor necrosis factor-α; NF-κB, nuclear
factor κ-light-chain-enhancer of activated B cells.

Figure 6

Molecular mechanisms of Tanshinone
IIA in the treatment of cerebral ischemia-reperfusion injury and
stroke. BDNF, brain-derived neurotrophic factor; CAT, catalase;
CREB, CAMP response element binding protein; FoxO3, forkhead box
O3; HO-1, heme oxygenase 1; IL-6, interleukin-6; HMGB1, high
mobility group box 1; MDA, malondialdehyde; NF-κB, nuclear factor
kappa-light-chain-enhancer of activated B cells; Nrf2, nuclear
factor erythroid 2-related factor 2; PI3K, phosphatidylinositol 3
kinase; ROS, reactive oxygen species; SOD, superoxide dismutase;
TNF-α, tumor necrosis factor-α; TORC1, target of rapamycin complex
1; 8-OHdG, 8-Hydroxy-2'-deoxyguanosine.
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Copy and paste a formatted citation
Spandidos Publications style
Pei W, Lu P, Ding C, Li Y and Li Y: Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review). Int J Mol Med 57: 120, 2026.
APA
Pei, W., Lu, P., Ding, C., Li, Y., & Li, Y. (2026). Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review). International Journal of Molecular Medicine, 57, 120. https://doi.org/10.3892/ijmm.2026.5791
MLA
Pei, W., Lu, P., Ding, C., Li, Y., Li, Y."Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review)". International Journal of Molecular Medicine 57.5 (2026): 120.
Chicago
Pei, W., Lu, P., Ding, C., Li, Y., Li, Y."Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review)". International Journal of Molecular Medicine 57, no. 5 (2026): 120. https://doi.org/10.3892/ijmm.2026.5791
Copy and paste a formatted citation
x
Spandidos Publications style
Pei W, Lu P, Ding C, Li Y and Li Y: Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review). Int J Mol Med 57: 120, 2026.
APA
Pei, W., Lu, P., Ding, C., Li, Y., & Li, Y. (2026). Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review). International Journal of Molecular Medicine, 57, 120. https://doi.org/10.3892/ijmm.2026.5791
MLA
Pei, W., Lu, P., Ding, C., Li, Y., Li, Y."Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review)". International Journal of Molecular Medicine 57.5 (2026): 120.
Chicago
Pei, W., Lu, P., Ding, C., Li, Y., Li, Y."Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review)". International Journal of Molecular Medicine 57, no. 5 (2026): 120. https://doi.org/10.3892/ijmm.2026.5791
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