Evidence map›Paper›PMID 32933582›Full record

ArticleSkeletal muscle2020

Exercise enhances mitochondrial fission and mitophagy to improve myopathy following critical limb ischemia in elderly mice via the PGC1a/FNDC5/irisin pathway.

Wuyang He, Peng Wang, Qingwei Chen, Chunqiu Li

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  3. Article
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  7. Leveraging mitochondrial stress to improve healthy aging.Sports medicine and health science · 2026
    Review
  8. Article
  9. Skeletal Muscle as Endocrine Organ.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Role of irisin in bone diseases.Frontiers in endocrinology · 2023
    Review
  18. Review
  19. Irisin, an Effective Treatment for Cardiovascular Diseases?Journal of cardiovascular development and disease · 2022
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Wuyang HeDepartment of Oncology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Peng WangDepartment of Geriatric Cardiology, The Second Affiliated Hospital of Chongqing Medical University, No. 76 Linjiang Road, Chongqing, 400010, China.
Qingwei ChenDepartment of Geriatric Cardiology, The Second Affiliated Hospital of Chongqing Medical University, No. 76 Linjiang Road, Chongqing, 400010, China. chenqwcq@sohu.com.
Chunqiu LiDepartment of Geriatric Cardiology, The Second Affiliated Hospital of Chongqing Medical University, No. 76 Linjiang Road, Chongqing, 400010, China.
Chongqing Medical University · CNDalian Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElderly populations are susceptible to critical limb ischemia (CLI), but conventional treatments cannot significantly decrease amputation and mortality. Although exercise is an effective "non-pharmacological medicine" targeting mitochondria to improve skeletal muscle function, few studies have focused on the application of exercise in CLI.

methodsElderly male C57BL/6 mice (14 months old) were used to establish a CLI model to assess the effect of exercise on perfusion, performance recovery, apoptosis, mitochondrial function, and mitochondrial turnover in gastrocnemius muscle. The potential underlying mechanism mediated by PGC1a/FNDC5/irisin was confirmed in hypoxic and nutrient-deprived myotubes undergoing electrical pulse stimuli (EPS).

resultsExercise significantly accelerated the perfusion recovery and exercise performance in ischemic limbs following CLI. Exercise improved the mitochondrial membrane potential and total ATP production and decreased apoptosis in the ischemic limbs. Exercise increased the formation of mitochondrial derived vesicle-like structures and decreased the mitochondrial length in the ischemic limbs, accompanied by upregulated PGC1a/FNDC5/irisin expression. In vitro, PGC1a/FNDC5/irisin downregulation decreased EPS-elevated PINK1, Parkin, DRP1, and LC3B mRNA levels. The irisin levels in the culture medium were correlated with the expression of mitochondrial fission and mitophagy markers in myotubes.

conclusionExercise enhanced mitochondrial fission and selective autophagy to promote the recovery of myopathy after CLI in elderly mice through the PGC1a/FNDC5/irisin pathway, supporting the efficacy of exercise therapy in elderly individuals with CLI and demonstrating the potential of targeting PGC1a/FNDC5/irisin as a new strategy for the treatment of CLI.

Indexed as

Mitochondrial DynamicsMitophagyMotor ActivityAnimalsCell HypoxiaCell LineFibronectinsIschemiaMaleMiceMice, Inbred C57BLMitochondria, MuscleMuscle, SkeletalMuscular DiseasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaFibronectinsFNDC5 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCritical limb ischemiaExerciseMitochondrial turnoverPGC1aSkeletal muscle

Identifiers

PMID32933582
PMCPMC7490877
OpenAlexW3085948910

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.