PGC1α overexpression preserves muscle mass and function in cisplatin‐induced cachexia
Background Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal mu...
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| Veröffentlicht in: | Journal of cachexia, sarcopenia and muscle Jg. 13; H. 5; S. 2480 - 2491 |
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| Hauptverfasser: | , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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John Wiley & Sons, Inc
01.10.2022
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| ISSN: | 2190-5991, 2190-6009, 2190-6009 |
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| Abstract | Background
Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin.
Methods
Young (2 month) and old (18 month) wild‐type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5–9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins.
Results
Young WT + C mice displayed reduced gastrocnemius mass (male: −16%, P < 0.0001; female: −11%, P < 0.001), muscle force (−6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: −53%, P < 0.01; female: −51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: −22%, P < 0.05; female: −27%, P < 0.05), muscle weakness (male: −20%, P < 0.0001; female: −17%, P < 0.01), and loss of MUNE (male: −82%, P < 0.01; female: −62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3‐fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow‐up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin‐induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome‐C, and Cox IV.
Conclusions
In our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria‐targeted strategies may serve as a tool to prevent chemotherapy‐induced muscle wasting and weakness. |
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| AbstractList | Abstract Background Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin. Methods Young (2 month) and old (18 month) wild‐type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5–9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins. Results Young WT + C mice displayed reduced gastrocnemius mass (male: −16%, P < 0.0001; female: −11%, P < 0.001), muscle force (−6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: −53%, P < 0.01; female: −51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: −22%, P < 0.05; female: −27%, P < 0.05), muscle weakness (male: −20%, P < 0.0001; female: −17%, P < 0.01), and loss of MUNE (male: −82%, P < 0.01; female: −62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3‐fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow‐up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin‐induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome‐C, and Cox IV. Conclusions In our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria‐targeted strategies may serve as a tool to prevent chemotherapy‐induced muscle wasting and weakness. Chemotherapy induces a cachectic-like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin.BACKGROUNDChemotherapy induces a cachectic-like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin.Young (2 month) and old (18 month) wild-type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5-9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins.METHODSYoung (2 month) and old (18 month) wild-type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5-9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins.Young WT + C mice displayed reduced gastrocnemius mass (male: -16%, P < 0.0001; female: -11%, P < 0.001), muscle force (-6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: -53%, P < 0.01; female: -51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: -22%, P < 0.05; female: -27%, P < 0.05), muscle weakness (male: -20%, P < 0.0001; female: -17%, P < 0.01), and loss of MUNE (male: -82%, P < 0.01; female: -62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3-fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow-up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin-induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome-C, and Cox IV.RESULTSYoung WT + C mice displayed reduced gastrocnemius mass (male: -16%, P < 0.0001; female: -11%, P < 0.001), muscle force (-6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: -53%, P < 0.01; female: -51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: -22%, P < 0.05; female: -27%, P < 0.05), muscle weakness (male: -20%, P < 0.0001; female: -17%, P < 0.01), and loss of MUNE (male: -82%, P < 0.01; female: -62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3-fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow-up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin-induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome-C, and Cox IV.In our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria-targeted strategies may serve as a tool to prevent chemotherapy-induced muscle wasting and weakness.CONCLUSIONSIn our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria-targeted strategies may serve as a tool to prevent chemotherapy-induced muscle wasting and weakness. BackgroundChemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin.MethodsYoung (2 month) and old (18 month) wild‐type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5–9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins.ResultsYoung WT + C mice displayed reduced gastrocnemius mass (male: −16%, P < 0.0001; female: −11%, P < 0.001), muscle force (−6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: −53%, P < 0.01; female: −51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: −22%, P < 0.05; female: −27%, P < 0.05), muscle weakness (male: −20%, P < 0.0001; female: −17%, P < 0.01), and loss of MUNE (male: −82%, P < 0.01; female: −62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3‐fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow‐up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin‐induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome‐C, and Cox IV.ConclusionsIn our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria‐targeted strategies may serve as a tool to prevent chemotherapy‐induced muscle wasting and weakness. Background Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin. Methods Young (2 month) and old (18 month) wild‐type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5–9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins. Results Young WT + C mice displayed reduced gastrocnemius mass (male: −16%, P < 0.0001; female: −11%, P < 0.001), muscle force (−6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: −53%, P < 0.01; female: −51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: −22%, P < 0.05; female: −27%, P < 0.05), muscle weakness (male: −20%, P < 0.0001; female: −17%, P < 0.01), and loss of MUNE (male: −82%, P < 0.01; female: −62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3‐fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow‐up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin‐induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome‐C, and Cox IV. Conclusions In our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria‐targeted strategies may serve as a tool to prevent chemotherapy‐induced muscle wasting and weakness. Chemotherapy induces a cachectic-like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α), a regulator of mitochondrial biogenesis, is often reduced in cachectic skeletal muscle. Overexpression of PGC1α has yielded mixed beneficial results in cancer cachexia, yet investigations using such approach in a chemotherapy setting are limited. Utilizing transgenic mice, we assessed whether overexpression of PGC1α could combat the skeletal muscle consequences of cisplatin. Young (2 month) and old (18 month) wild-type (WT) and PGC1α transgenic male and female mice (Tg) were injected with cisplatin (C; 2.5 mg/kg) for 2 weeks, while control animals received saline (n = 5-9/group). Animals were assessed for muscle mass and force, motor unit connectivity, and expression of mitochondrial proteins. Young WT + C mice displayed reduced gastrocnemius mass (male: -16%, P < 0.0001; female: -11%, P < 0.001), muscle force (-6%, P < 0.05, both sexes), and motor unit number estimation (MUNE; male: -53%, P < 0.01; female: -51%, P < 0.01). Old WT + C male and female mice exhibited gastrocnemius wasting (male: -22%, P < 0.05; female: -27%, P < 0.05), muscle weakness (male: -20%, P < 0.0001; female: -17%, P < 0.01), and loss of MUNE (male: -82%, P < 0.01; female: -62%, P < 0.05), suggesting exacerbated cachexia compared with younger animals. Overexpression of PGC1α had mild protective effects on muscle mass in young Tg + C male only (gastrocnemius: +10%, P < 0.05); however, force and MUNE were unchanged in both young Tg + C male and female, suggesting preservation of neuromuscular function. In older male, protective effects associated with PGC1α overexpression were heighted with Tg + C demonstrating preserved muscle mass (gastrocnemius: +34%, P < 0.001), muscle force (+13%, P < 0.01), and MUNE (+3-fold, P < 0.05). Similarly, old female Tg + C did not exhibit muscle wasting or reductions in MUNE, and had preserved muscle force (+11%, P < 0.05) compared with female WT + C. Follow-up molecular analysis demonstrated that aged WT animals were more susceptible to cisplatin-induced loss of mitochondrial proteins, including PGC1α, OPA1, cytochrome-C, and Cox IV. In our study, the negative effects of cisplatin were heighted in aged animals, whereas overexpression of PGC1α was sufficient to combat the neuromuscular dysfunction caused by cisplatin, especially in older animals. Hence, our observations indicate that aged animals may be more susceptible to develop chemotherapy side toxicities and that mitochondria-targeted strategies may serve as a tool to prevent chemotherapy-induced muscle wasting and weakness. |
| Author | Bonetto, Andrea Pin, Fabrizio Huot, Joshua R. Chatterjee, Rohit |
| AuthorAffiliation | 1 Department of Surgery Indiana University School of Medicine Indianapolis IN USA 3 Department of Otolaryngology – Head & Neck Surgery Indiana University School of Medicine Indianapolis IN USA 2 Department of Anatomy, Cell Biology & Physiology Indiana University School of Medicine Indianapolis IN USA 4 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis IN USA 5 Simon Comprehensive Cancer Center Indiana University School of Medicine Indianapolis IN USA |
| AuthorAffiliation_xml | – name: 2 Department of Anatomy, Cell Biology & Physiology Indiana University School of Medicine Indianapolis IN USA – name: 4 Indiana Center for Musculoskeletal Health Indiana University School of Medicine Indianapolis IN USA – name: 5 Simon Comprehensive Cancer Center Indiana University School of Medicine Indianapolis IN USA – name: 3 Department of Otolaryngology – Head & Neck Surgery Indiana University School of Medicine Indianapolis IN USA – name: 1 Department of Surgery Indiana University School of Medicine Indianapolis IN USA |
| Author_xml | – sequence: 1 givenname: Joshua R. surname: Huot fullname: Huot, Joshua R. organization: Indiana University School of Medicine – sequence: 2 givenname: Fabrizio surname: Pin fullname: Pin, Fabrizio organization: Indiana University School of Medicine – sequence: 3 givenname: Rohit surname: Chatterjee fullname: Chatterjee, Rohit organization: Indiana University School of Medicine – sequence: 4 givenname: Andrea orcidid: 0000-0002-3235-1871 surname: Bonetto fullname: Bonetto, Andrea email: abonetto@iu.edu organization: Indiana University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35903870$$D View this record in MEDLINE/PubMed |
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| Copyright | 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. 2022. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1002/jcsm.13035 |
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| Keywords | Chemotherapy PGC1α Cisplatin Skeletal muscle cachexia |
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Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome... Chemotherapy induces a cachectic-like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome... BackgroundChemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome... Abstract Background Chemotherapy induces a cachectic‐like phenotype, accompanied by skeletal muscle wasting, weakness and mitochondrial dysfunction. Peroxisome... |
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| SubjectTerms | Age Animals Antineoplastic Agents Body composition cachexia Cachexia - etiology Cancer Chemotherapy Cisplatin Cisplatin - adverse effects Connectivity Cytochromes - metabolism Cytochromes - pharmacology Female Infrared imaging systems Laboratory animals Male Mice Mice, Transgenic Mitochondrial Proteins - metabolism Muscle function Muscle, Skeletal - pathology Muscular Atrophy - etiology Musculoskeletal system Original Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - pharmacology Peroxisome Proliferator-Activated Receptors - metabolism Peroxisome Proliferator-Activated Receptors - pharmacology PGC1α Proteins Skeletal muscle Variance analysis |
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| Title | PGC1α overexpression preserves muscle mass and function in cisplatin‐induced cachexia |
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