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Article Open Access

CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats

  • Authors:
    • Tianzhu Liu
    • Longqing Zhang
    • Wei Mei
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 197
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    Published online on: May 21, 2026
       https://doi.org/10.3892/ijmm.2026.5868
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Abstract

Neuropathic pain arises from an intricate network of interconnected pathophysiological mechanisms, yet the arsenal of effective therapeutic strategies remains frustratingly limited. Accumulating evidence has linked mitochondrial dysfunction to the progression of neuropathic pain. C1q‑tumor necrosis factor‑related protein‑3 (CTRP3), a newly identified adipokine with diverse cytoprotective capacities, has not been previously explored for its role in nociceptive processing. To explore the role of CTRP3 in pain hypersensitivity, pain‑related behavioral assessments were conducted using von Frey filaments and acetone drop method in male rats subjected to spared nerve injury (SNI). To unravel the underlying mechanisms, spinal cord tissues were subjected to western blotting, reverse transcription‑quantitative PCR, immunofluorescence staining, dihydroethidium staining, small interfering RNA (siRNA) technologies and biochemical assays for quantifying oxidative markers. The findings showed that SNI markedly reduced endogenous CTRP3 expression in spinal neurons. Intrathecal administration of recombinant CTRP3 (rCTRP3) alleviated mechanical allodynia and cold hyperalgesia in SNI‑induced rats. Additionally, rCTRP3 treatment enhanced PGC‑1α‑mediated mitochondrial biogenesis, ATF5‑triggered mitochondrial unfolded protein response (UPRmt), and mitigated spinal oxidative stress. Mechanistically, pharmacological inhibition of SIRT1 with EX‑527, or siRNA‑mediated silencing of PGC‑1α or ATF5, reversed the effects of CTRP3 on pain hypersensitivity, mitochondrial biogenesis, UPRmt and oxidative stress. The present study demonstrates that CTRP3 mitigates mechanical allodynia and cold hyperalgesia in male SNI rats by activating spinal SIRT1, thereby enhancing PGC‑1α‑mediated mitochondrial biogenesis and ATF5‑induced UPRmt. CTRP3 may therefore represent a novel therapeutic target for the management of neuropathic pain.
View Figures

Figure 1

Spinal CTRP3 expression is
downregulated following SNI. (A and B) Compared with sham-operated
control rats, rats subjected to SNI exhibited a significant
reduction in PWT and a prominent elevation in PWCD from post-SNI
day 3 to day 14. ****P<0.0001 vs. sham group, n=10
rats/group. (C and D) RT-qPCR and WB analyses showed a marked
decrease in CTRP3 mRNA and protein levels in the spinal cord of SNI
rats relative to sham controls. (E-I) IF staining results
demonstrated that SNI led to reduced CTRP3 expression in neurons
within the spinal dorsal horn of rats. ****P<0.0001
vs. sham group, n=5 rats/group. SNI, spared nerve injury; PWT, paw
withdrawal threshold; PWCD, paw withdrawal cold duration; RT-qPCR,
reverse transcription-quantitative polymerase chain reaction; WB,
western blotting; IF, immunofluorescence; CTRP3, C1q-tumor necrosis
factor-related protein 3.

Figure 2

Intrathecal administration of rCTRP3
alleviates pain hypersensitivity and activates spinal SIRT1 in SNI
rats. (A and B) Behavioral assessments showed that repeated
intrathecal injection of rCTRP3 (30 or 90 μg) significantly
reversed the SNI-induced reductions in PWT and increases in PWCD.
****P<0.0001 vs. sham group; ##P<0.01,
###P<0.001 and ####P<0.0001 vs. SNI +
vehicle group; n=10 rats/group. (C and D) IF staining results
revealed that the number of SIRT1-positive neurons was lower in SNI
rats than in the sham group, whereas treatment with rCTRP3 (30 and
90 μg) reversed this decrease in SIRT1 expression in spinal
dorsal horn neurons of SNI rats. (E) WB analysis demonstrated that
SIRT1 levels in the spinal cord were reduced in SNI rats, and this
downregulation was markedly attenuated by rCTRP3 treatment at doses
of 30 or 90 μg. **P<0.01 and
***P<0.001 vs. sham group; ##P<0.01 and
###P<0.001, vs. SNI + vehicle group; n=5 rats/group.
rCTRP3, recombinant complement C1q tumor necrosis factor-related
protein 3; SNI, spared nerve injury; PWT, paw withdrawal threshold;
PWCD, paw withdrawal cold duration; IF, immunofluorescence; SIRT1,
sirtuin 1; WB, western blotting.

Figure 3

rCTRP3 promotes PGC-1α-mediated
mitochondrial biogenesis in the spinal cord of SNI rats. (A and B)
IF staining showed a significant decrease in neuronal PGC-1α levels
in SNI rats; this reduction was notably reversed by intrathecal
administration of rCTRP3 (30 and 90 μg). (C-E) WB analysis
demonstrated that rCTRP3 treatment (30 and 90 μg) blocked
the nerve injury-induced downregulation of PGC-1α, NRF1 and TFAM in
the spinal cord, compared with the SNI + vehicle group. (F) rCTRP3
administration (30 and 90 μg) reversed the reduction in
spinal mtDNA copy number observed in SNI rats.
***P<0.001 vs. sham group; ##P<0.01,
###P<0.001 and ####P<0.0001 vs. SNI +
vehicle group; n=5 rats/group. rCTRP3, recombinant complement C1q
tumor necrosis factor-related protein 3; PGC-1α, peroxisome
proliferator-activated receptor gamma coactivator 1-alpha; SNI,
spared nerve injury; IF, immunofluorescence; WB, western blotting;
NRF1, nuclear respiratory factor 1; TFAM, mitochondrial
transcription factor A; mtDNA, mitochondrial DNA.

Figure 4

rCTRP3 promotes ATF5-induced
UPRmt in the spinal cord of SNI rats. (A and B) IF
staining showed a notable decrease in spinal neuronal ATF5 levels
in SNI rats; this reduction was significantly reversed by
intrathecal administration of rCTRP3 (30 and 90 μg). (C-F)
RT-qPCR analysis demonstrated that rCTRP3 treatment (30 and 90
μg) blocked the nerve injury-induced downregulation of ATF5,
ClpP, Hsp60 and LonP1 in the spinal cord, compared with the SNI +
vehicle group. **P<0.01 and ***P<0.001
vs. sham group; #P<0.05, ##P<0.01,
###P<0.001 and ####P<0.0001 vs. SNI +
vehicle group; n=5 rats/group. rCTRP3, recombinant complement C1q
tumor necrosis factor-related protein 3; ATF5, activating
transcription factor 5; UPRmt, mitochondrial unfolded
protein response; SNI, spared nerve injury; IF, immunofluorescence;
RT-qPCR, reverse transcription-quantitative polymerase chain
reaction; ClpP, caseinolytic mitochondrial matrix peptidase
proteolytic subunit; Hsp60, heat shock protein 60; LonP1, Lon
protease 1.

Figure 5

rCTRP3 administration attenuates
SNI-induced oxidative stress in the rat spinal cord. (A and B) DHE
staining showed that rCTRP3 treatment (30 and 90 μg)
significantly reduced the increased number of DHE-positive cells in
the spinal dorsal horn of SNI rats. (C and D) Biochemical assays
revealed that SNI elevated the spinal content of MDA and PCO;
intrathecal injection of rCTRP3 (30 and 90 μg) reversed this
elevation. (E and F) rCTRP3 (30 and 90 μg) restored the
reduced concentrations of reduced GSH and activity of GSH-PX in the
spinal cord of SNI rats. (G) Administration of rCTRP3 (30 and 90
μg) reversed the decreased activity of SOD in the spinal
cord of SNI rats. **P<0.01, ***P<0.001
and ****P<0.0001 vs. sham group;
##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group; n=5 rats/group.
rCTRP3, recombinant complement C1q tumor necrosis factor-related
protein 3; SNI, spared nerve injury; DHE, dihydroethidium; MDA,
malondialdehyde; PCO, protein carbonyl; GSH, glutathione; GSH-PX,
glutathione peroxidase; SOD, superoxide dismutase.

Figure 6

SIRT1 antagonist abrogates
rCTRP3-mediated amelioration of pain hypersensitivity and
PGC-1α-dependent mitochondrial biogenesis in SNI rats. (A and B)
Intrathecal injection of EX-527 (a SIRT1 antagonist) reversed the
rCTRP3-induced increases in PWT and reductions in PWCD in SNI rats.
****P<0.0001 vs. sham group; ###P<0.001
and ####P<0.0001 vs. SNI + vehicle group;
&&P<0.01 and
&&&P<0.001 vs. SNI + rCTRP3 group; n=10
rats/group. (C and D) IF staining revealed that EX-527 blocked the
rCTRP3-induced upregulation of PGC-1α expression in spinal dorsal
horn neurons of SNI rats. (E-G) WB analysis demonstrated that
EX-527 abolished the rCTRP3-mediated elevation of PGC-1α, NRF1 and
TFAM levels in the spinal cord of SNI rats. (H) Administration of
rCTRP3 reversed the reduction in mtDNA copy number in SNI rats, but
this protective effect was inhibited by EX-527.
*P<0.05, ***P<0.001 and
****P<0.0001 vs. sham group; #P<0.05,
##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group;
&&P<0.01,
&&&P<0.001 and
&&&&P<0.0001 vs. SNI + rCTRP3 group;
n=5 rats/group. SIRT1, sirtuin 1; rCTRP3, recombinant complement
C1q tumor necrosis factor-related protein 3; SNI, spared nerve
injury; EX-527, a selective SIRT1 antagonist; PWT, paw withdrawal
threshold; PWCD, paw withdrawal cold duration; IF,
immunofluorescence; WB, Western blotting; PGC-1α, peroxisome
proliferator-activated receptor gamma coactivator 1-alpha; NRF1,
nuclear respiratory factor 1; TFAM, mitochondrial transcription
factor A; mtDNA, mitochondrial DNA.

Figure 7

SIRT1 antagonist blocks
rCTRP3-induced enhancement of ATF5-mediated UPRmt in SNI
rats. (A and B) IF staining results showed that EX-527 inhibited
the rCTRP3-induced upregulation of ATF5 expression in spinal dorsal
horn neurons of SNI rats. (C-F) RT-qPCR analysis demonstrated that
EX-527 abolished the rCTRP3-mediated elevation of ATF5, ClpP, Hsp60
and LonP1 expression in the spinal cord, compared with the SNI +
rCTRP3 group. **P<0.01, ***P<0.001 and
****P<0.0001 vs. sham group; ##P<0.01
and ###P<0.001 vs. SNI + vehicle group;
&&P<0.01 and
&&&P<0.001 vs. SNI + rCTRP3 group; n=5
rats/group. SIRT1, sirtuin 1; rCTRP3, recombinant complement C1q
tumor necrosis factor-related protein 3; SNI, spared nerve injury;
EX-527, selective SIRT1 inhibitor; IF, immunofluorescence; RT-qPCR,
reverse transcription-quantitative polymerase chain reaction; ATF5,
activating transcription factor 5; UPRmt, mitochondrial
unfolded protein response; ClpP, caseinolytic mitochondrial matrix
peptidase proteolytic subunit; Hsp60, heat shock protein 60; LonP1,
Lon protease 1.

Figure 8

SIRT1 inhibitor abrogates
rCTRP3-induced attenuation of spinal oxidative stress in SNI rats.
(A and B) DHE staining revealed that, compared with the SNI +
rCTRP3 group, EX-527 treatment reversed the rCTRP3-induced decrease
in the number of DHE-positive cells in the spinal cord of SNI rats.
(C and D) Biochemical assay results demonstrated that EX-527
eliminated the rCTRP3-mediated reduction in spinal levels of MDA
and PCO in SNI rats. (E-G) rCTRP3 treatment increased the spinal
level of reduced GSH and enhanced the activity of GSH-PX and SOD in
SNI rats; however, these protective effects were counteracted by
the SIRT1 antagonist (EX-527). *P<0.05,
**P<0.01, ***P<0.001 and
****P<0.0001 vs. sham group; #P<0.05,
##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group;
&&P<0.01,
&&&P<0.001 and
&&&&P<0.0001 vs. SNI + rCTRP3 group;
n=5 rats/group. SIRT1, sirtuin 1; rCTRP3, recombinant complement
C1q tumor necrosis factor-related protein 3; SNI, spared nerve
injury; EX-527, a selective SIRT1 inhibitor; DHE, dihydroethidium;
MDA, malondialdehyde; PCO, protein carbonyl; GSH, glutathione;
GSH-PX, glutathione peroxidase; SOD, superoxide dismutase.

Figure 9

PGC-1α siRNA abrogates
rCTRP3-mediated alleviation of pain hypersensitivity in SNI rats.
(A) RT-qPCR analysis confirmed that PGC-1α siRNA transfection
induced significant downregulation of PGC-1α mRNA in PC12 cells.
***P<0.001 vs. negative siRNA group; n=5. (B) RT-qPCR
results verified that PGC-1α siRNA efficiently suppressed PGC-1α
expression in the spinal cord. ***P<0.001 vs.
negative siRNA group; n=5 rats/group. (C and D) Behavioral
assessments showed that rCTRP3 treatment increased PWT and reduced
PWCD in SNI rats; however, co-administration of PGC-1α siRNA
reversed this analgesic effect of rCTRP3.
****P<0.0001 vs. sham group; ##P<0.01,
###P<0.001 and ####P<0.0001 vs. SNI +
vehicle group; &&P<0.01 and
&&&P<0.001 vs. SNI + rCTRP3 group; n=10
rats/group. PGC-1α, peroxisome proliferator-activated receptor
gamma coactivator 1-alpha; siRNA, small interfering RNA; rCTRP3,
recombinant complement C1q tumor necrosis factor-related protein 3;
SNI, spared nerve injury; RT-qPCR, reverse
transcription-quantitative polymerase chain reaction; PWT, paw
withdrawal threshold; PWCD, paw withdrawal cold duration.

Figure 10

PGC-1α siRNA abrogates
rCTRP3-mediated enhancement of mitochondrial biogenesis in SNI
rats. (A and B) IF staining revealed that PGC-1α siRNA blocked the
rCTRP3-induced upregulation of PGC-1α expression in spinal dorsal
horn neurons of SNI rats. (C-E) WB analysis demonstrated that
PGC-1α siRNA eliminated the rCTRP3-mediated elevation of PGC-1α,
NRF1, and TFAM levels in the spinal cord, compared with the SNI +
rCTRP3 group. (F) rCTRP3 treatment reversed the reduction in mtDNA
copy number in SNI rats, and this regulatory effect was inhibited
by PGC-1α siRNA. *P<0.05, ***P<0.001
and ****P<0.0001 vs. sham group;
##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group;
&P<0.05, &&P<0.01,
&&&P<0.001 and
&&&&P<0.0001 vs. SNI + rCTRP3 group;
n=5 rats/group. PGC-1α, peroxisome proliferator-activated receptor
gamma coactivator 1-alpha; siRNA, small interfering RNA; rCTRP3,
recombinant complement C1q tumor necrosis factor-related protein 3;
SNI, spared nerve injury; IF, immunofluorescence; WB, Western
blotting; NRF1, nuclear respiratory factor 1; TFAM, mitochondrial
transcription factor A; mtDNA, mitochondrial DNA.

Figure 11

PGC-1α siRNA blocks rCTRP3-induced
reduction of spinal oxidative stress in SNI rats. (A and B) DHE
staining analysis showed that compared with the SNI + rCTRP3 group,
administration of PGC-1α siRNA reversed the rCTRP3-induced decrease
in the number of DHE-positive cells in the spinal cord of SNI rats.
(C and D) Biochemical assay results revealed that PGC-1α siRNA
abolished the rCTRP3-mediated downregulation of MDA and PCO, in the
spinal cord of SNI rats. (E-G) Administration of rCTRP3 increased
the level of reduced GSH and enhanced the activity of GSH-PX and
SOD in the spinal cord of SNI rats, but these beneficial changes
were counteracted by PGC-1α siRNA intervention.
***P<0.001 and ****P<0.0001 vs. sham
group; ##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group;
&P<0.05, &&P<0.01,
&&&P<0.001 and
&&&&P<0.0001 vs. SNI + rCTRP3 group;
n=5 rats/group. PGC-1α, peroxisome proliferator-activated receptor
gamma coactivator 1-alpha; siRNA, small interfering RNA; rCTRP3,
recombinant complement C1q tumor necrosis factor-related protein 3;
SNI, spared nerve injury; DHE, dihydroethidium; MDA,
malondialdehyde; PCO, protein carbonyl; GSH, glutathione; GSH-PX,
glutathione peroxidase; SOD, superoxide dismutase.

Figure 12

ATF5 siRNA abrogates rCTRP3-mediated
alleviation of pain hypersensitivity in SNI rats. (A) RT-qPCR
analysis confirmed that ATF5 siRNA transfection induced significant
downregulation of ATF5 mRNA in PC12 cells.
****P<0.0001 vs. negative siRNA group; n=5. (B)
RT-qPCR results confirmed that ATF5 siRNA effectively inhibited
ATF5 expression in the spinal cord. ***P<0.001 vs.
negative siRNA group; n=5 rats/group. (C and D) Behavioral
assessments demonstrated that rCTRP3 treatment elevated PWT and
downregulated PWCD in SNI rats; however, co-administration of ATF5
siRNA reversed this analgesic effect of rCTRP3.
****P<0.0001 vs. sham group; ##P<0.01,
###P<0.001 and ####P<0.0001 vs. SNI +
vehicle group; &P<0.05,
&&P<0.01 and
&&&P<0.001 vs. SNI + rCTRP3 group; n=10
rats/group. ATF5, activating transcription factor 5; siRNA, small
interfering RNA; rCTRP3, recombinant complement C1q tumor necrosis
factor-related protein; SNI, spared nerve injury; RT-qPCR, reverse
transcription-quantitative polymerase chain reaction; PWT, paw
withdrawal threshold; PWCD, paw withdrawal cold duration.

Figure 13

ATF5 siRNA abrogates rCTRP3-mediated
enhancement of UPRmt in SNI rats. (A and B) IF staining
revealed that ATF5 siRNA inhibited the rCTRP3-induced upregulation
of ATF5 expression in spinal dorsal horn neurons of SNI rats. (C-F)
RT-qPCR analysis demonstrated that ATF5 siRNA eliminated the
rCTRP3-mediated elevation in the expression levels of ATF5, ClpP,
Hsp60 and LonP1 in the spinal cord, relative to the SNI + rCTRP3
group. **P<0.01, ***P<0.001 and
****P<0.0001 vs. sham group; ##P<0.01
and ###P<0.001 vs. SNI + vehicle group;
&P<0.05 and &&P<0.01 vs.
SNI + rCTRP3 group; n=5 rats/group. ATF5, activating transcription
factor 5; siRNA, small interfering RNA; rCTRP3, recombinant
complement C1q tumor necrosis factor-related protein;
UPRmt, mitochondrial unfolded protein response; SNI,
spared nerve injury; IF, immunofluorescence; RT-qPCR, reverse
transcription-quantitative polymerase chain reaction; ClpP,
caseinolytic mitochondrial matrix peptidase proteolytic subunit;
Hsp60, heat shock protein 60; LonP1, Lon protease 1.

Figure 14

ATF5 siRNA abrogates rCTRP3-induced
reduction of spinal oxidative stress in SNI rats. (A and B) DHE
staining analysis indicated that compared with the SNI + rCTRP3
group, administration of ATF5 siRNA counteracted the rCTRP3-induced
decrease in the number of DHE-positive cells in the spinal cord of
SNI rats. (C and D) Biochemical assay data revealed that ATF5 siRNA
abolished the rCTRP3-mediated downregulation of MDA and PCO in the
spinal cord of SNI rats. (E-G) rCTRP3 treatment increased the level
of reduced GSH, and enhanced the activity of GSH-PX and SOD in the
spinal cord of SNI rats, but these favorable changes were reversed
by ATF5 siRNA intervention. **P<0.01,
***P<0.001 and ****P<0.0001 vs. sham
group; ##P<0.01, ###P<0.001 and
####P<0.0001 vs. SNI + vehicle group;
&&P<0.01,
&&&P<0.001 and
&&&&P<0.0001 vs. SNI + rCTRP3 group;
n=5 rats/group. ATF5, activating transcription factor 5; siRNA,
small interfering RNA; rCTRP3, recombinant complement C1q tumor
necrosis factor-related protein; SNI, spared nerve injury; DHE,
dihydroethidium; MDA, malondialdehyde; PCO, protein carbonyl; GSH,
glutathione; GSH-PX, glutathione peroxidase; SOD, superoxide
dismutase.

Figure 15

Schematic illustration of the role of
CTRP3 in neuropathic pain. CTRP3 alleviates pain hypersensitivity
and spinal oxidative stress in SNI rats by activating spinal SIRT1,
thereby enhancing PGC-1α/ATF5-induced mitochondrial biogenesis and
UPRmt. CTRP3, complement C1q tumor necrosis
factor-related protein 3; SNI, spared nerve injury; SIRT1, sirtuin
1; PGC-1α, peroxisome proliferator-activated receptor gamma
coactivator 1-alpha; ATF5, activating transcription factor 5;
UPRmt, mitochondrial unfolded protein response; MDA,
malondialdehyde; PCO, protein carbonyl; MMP, mitochondrial membrane
potential; GSH, glutathione; GSH-PX, glutathione peroxidase; SOD,
superoxide dismutase; DHE, dihydroethidium; ClpP, caseinolytic
mitochondrial matrix peptidase proteolytic subunit; Hsp60, heat
shock protein 60; LonP1, Lon protease 1; siRNA, small interfering
RNA.
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Copy and paste a formatted citation
Spandidos Publications style
Liu T, Zhang L and Mei W: CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats. Int J Mol Med 58: 197, 2026.
APA
Liu, T., Zhang, L., & Mei, W. (2026). CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats. International Journal of Molecular Medicine, 58, 197. https://doi.org/10.3892/ijmm.2026.5868
MLA
Liu, T., Zhang, L., Mei, W."CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats". International Journal of Molecular Medicine 58.1 (2026): 197.
Chicago
Liu, T., Zhang, L., Mei, W."CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats". International Journal of Molecular Medicine 58, no. 1 (2026): 197. https://doi.org/10.3892/ijmm.2026.5868
Copy and paste a formatted citation
x
Spandidos Publications style
Liu T, Zhang L and Mei W: CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats. Int J Mol Med 58: 197, 2026.
APA
Liu, T., Zhang, L., & Mei, W. (2026). CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats. International Journal of Molecular Medicine, 58, 197. https://doi.org/10.3892/ijmm.2026.5868
MLA
Liu, T., Zhang, L., Mei, W."CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats". International Journal of Molecular Medicine 58.1 (2026): 197.
Chicago
Liu, T., Zhang, L., Mei, W."CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats". International Journal of Molecular Medicine 58, no. 1 (2026): 197. https://doi.org/10.3892/ijmm.2026.5868
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