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Cited by 295Muscle Physiology and DisordersAdipose Tissue and MetabolismMitochondrial Function and Pathology

The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.

Role of PGC-1α Signaling in Skeletal Muscle Health and Disease

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Kang, Chounghun, Li Ji, Li·2012·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2012.06738.xPMC PMC3499658
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Abstract

This paper reviews the current understanding of the molecular basis of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-mediated pathway and discusses the role of PGC-1α in skeletal muscle atrophy caused by immobilization. PGC-1α is the master transcription regulator that stimulates mitochondrial biogenesis, by upregulating nuclear respiratory factors (NRF-1, 2) and mitochondrial transcription factor A (Tfam), which leads to increased mitochondrial DNA replication and gene transcription. PGC-1α also regulates cellular oxidant-antioxidant homeostasis by stimulating the gene expression of superoxide dismutase-2 (SOD2), catalase, glutathione peroxidase 1 (GPx1), and uncoupling protein (UCP). Recent reports from muscle-specific PGC-1α overexpression underline the importance of PGC-1α in atrophied skeletal muscle, demonstrate enhancement of the PGC-1α mitochondrial biogenic pathway, and reduced oxidative damage. Thus, PGC-1α appears to play a protective role against atrophy-linked skeletal muscle deterioration.

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Crossref · 10.1111/j.1749-6632.2012.06738.x

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Figures

Figure 1 Regulation of PGC-1α gene expression. PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Tfam, mitochondria transcription factor A; MAPK, mitogen-activated protein kinase; MKK6, MAP kinase kinase: CaMK, calcium/calmodulin-dependent protein kinase; CREB, cyclic AMP response element binding protein; MEF, myocyte enhancer factor; ATF, activating transcription factor; NRF, nuclear respiratory factor; ERR, estrogen-related receptor; XO, xanthine oxidase; PKC, protein kinase C. (Figure modified from Ref. 7.)
Figure 1 Regulation of PGC-1α gene expression. PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Tfam, mitochondria transcription factor A; MAPK, mitogen-activated protein kinase; MKK6, MAP kinase kinase: CaMK, calcium/calmodulin-dependent protein kinase; CREB, cyclic AMP response element binding protein; MEF, myocyte enhancer factor; ATF, activating transcription factor; NRF, nuclear respiratory factor; ERR, estrogen-related receptor; XO, xanthine oxidase; PKC, protein kinase C. (Figure modified from Ref. 7.)CC BY · PubMed Central
Figure 2 Western blot analysis of PGC-1α and actin protein contents in rat deep vastuslateralis (DVL) muscle. Data were expressed as the ratio of densitometric intensity of PGC-1α and actin protein bend. Exer, treadmill running for 88 minutes; ALP, allopurinol injection 1 and 24 h prior to exercise. **P < 0.01, exer or exer + ALP versus control; ++P < 0.01, exer + ALP versus exer.
Figure 2 Western blot analysis of PGC-1α and actin protein contents in rat deep vastuslateralis (DVL) muscle. Data were expressed as the ratio of densitometric intensity of PGC-1α and actin protein bend. Exer, treadmill running for 88 minutes; ALP, allopurinol injection 1 and 24 h prior to exercise. **P < 0.01, exer or exer + ALP versus control; ++P < 0.01, exer + ALP versus exer.CC BY · PubMed Central
Figure 3 Aging affects of PGC-1α on rat soleus muscle. Twelve weeks of endurance training restores PGC-1α protein contents. Western blot detection of PGC-1α normalized with actin protein content. Each bar represents mean ± SEM (N= 3). **P < 0.01; young (Y) versus old (O) or old training (OT), ††P < 0.01; old (O) versus old training (OT). Three groups of Fischer 344/BNF1 rats (young, rested (Y, four months old, N= 3); old, rested (O, 24 months old, N= 3); and old, subjected to a 12-week treadmill running at 17.5 m/min, 10% grade for 45 min/day five days/week (OT, 24 months old, N= 3)).
Figure 3 Aging affects of PGC-1α on rat soleus muscle. Twelve weeks of endurance training restores PGC-1α protein contents. Western blot detection of PGC-1α normalized with actin protein content. Each bar represents mean ± SEM (N= 3). **P < 0.01; young (Y) versus old (O) or old training (OT), ††P < 0.01; old (O) versus old training (OT). Three groups of Fischer 344/BNF1 rats (young, rested (Y, four months old, N= 3); old, rested (O, 24 months old, N= 3); and old, subjected to a 12-week treadmill running at 17.5 m/min, 10% grade for 45 min/day five days/week (OT, 24 months old, N= 3)).CC BY · PubMed Central
Figure 4 Effect of PGC-1α overexpression on mitochondria content and function in mice atrophied muscles. Mitochondria DNA content (mtDNA/nDNA) and ATP production rate (MAPR) were determined in the FVB/N mice TA (tibialis anterior) muscles. Data are mean + SEM. *P < 0.05 IM-RM versus control; **P < 0.01 IM-RM versus control; +P < 0.05 PGC-1α versus GFP. IM-RM, 14 days immobilization plus 5-day remobilization.
Figure 4 Effect of PGC-1α overexpression on mitochondria content and function in mice atrophied muscles. Mitochondria DNA content (mtDNA/nDNA) and ATP production rate (MAPR) were determined in the FVB/N mice TA (tibialis anterior) muscles. Data are mean + SEM. *P < 0.05 IM-RM versus control; **P < 0.01 IM-RM versus control; +P < 0.05 PGC-1α versus GFP. IM-RM, 14 days immobilization plus 5-day remobilization.CC BY · PubMed Central

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  1. 10.1016/S0092-8674(00)80611-X · DOI · Paper page
  2. 10.1038/nature00904 · DOI · Paper page
  3. Kang C., 2012, PGC‐1α enhances skeletal muscle recovery from disuse atrophy, Med. Sci. Sports Exer., 44, S501

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Metadata

Authors
Kang, C., & Li Ji, L.
Affiliations
University of Minnesota (US)
ORCID
Kang, Chounghun
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2012-10
Volume
1271
Issue
1
Pages
110-117
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2012.06738.x
PMC
PMC3499658
OpenAlex
W1524273338
Cited by
291
References
60
Citations by year
2026: 24 · 2025: 32 · 2024: 35 · 2023: 31 · 2022: 20 · 2021: 30 · 2020: 30 · 2019: 17 · 2018: 18 · 2017: 12 · 2016: 9 · 2015: 15 · 2014: 11 · 2013: 7
FWCI
0.96
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 9 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
PGC-1α, skeletal muscle atrophy, immobilization, mitochondrial biogenesis, nuclear respiratory factors, TFAM, oxidative stress, antioxidant enzymes, manganese superoxide dismutase, uncoupling proteins, muscle health
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Aging, Animals, Heat-Shock Proteins, Humans, Muscular Atrophy, Musculoskeletal Diseases, Oxidoreductases, Transcription Factors, Signal Transduction, Exercise, Gene Expression Regulation, Enzymologic, Muscle, Skeletal, Mitochondrial Turnover

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