Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin

Gilson, Hélène; Schakman, Olivier; Kalista, Stéphanie; Lause, Pascale; Tsuchida, Kunihiro; Thissen, Jean‐Paul

doi:10.1152/ajpendo.00193.2009

Cited by 211 publications

(202 citation statements)

References 48 publications

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“…At baseline, deceased patients had a lower body mass index (24 kg/m 2 vs. 25 kg/m 2 , P = 0.026) and had lost more body weight (5.4% vs. 2.4%, P = 0.019) than alive patients. Moreover, deceased patients had more severe anorexia (SNAQ score: deceased vs. alive patients: 146, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 vs. 168, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20; P = 0.005), more symptoms (QLQ‐C30: deceased vs. alive patients: 33 2–66 vs. 15 6–69 ; P < 0.0001), a poorer quality of life (QLQ‐C30: deceased vs. alive patients: 58 16–100 vs. 66 0–100 ; P = 0.002) and a lower functional capacity (QLQ‐C30: deceased vs. alive patients: 64 18–97 vs. 82 33–100 ; P < 0.0001 and ECOG; P < 0.0001) than alive patients.…”

Section: Resultsmentioning

confidence: 99%

Circulating Activin A predicts survival in cancer patients

Loumaye

Barsy

Nachit

et al. 2017

J cachexia sarcopenia muscle

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BackgroundSeveral experimental evidences pinpoint the possible role of Activin A (ActA) as a driver of cancer cachexia. Supporting this hypothesis, we showed recently that human cancer cachexia is associated with high ActA levels. Moreover, ActA levels were correlated with body weight loss and skeletal muscle density, two prognostic factors in cancer patients. Our goal was therefore to investigate the value of ActA to predict survival in cancer patients.MethodsPatients with colorectal or lung cancer were prospectively enrolled at the time of diagnosis or relapse between January 2012 and March 2014. At baseline, patients had clinical, nutritional, and functional assessment. Body composition and skeletal muscle density were measured by CT scan, and plasma ActA concentrations were determined. Overall survival (OS) was analysed since inclusion to 24 months later.ResultsSurvival data were available for 149 patients out of 152. Patients with high ActA (≥408 pg/mL) had lower OS than those with low levels, regardless the type of cancer (OS in colorectal cancer, 50% vs. 79%, P < 0.05; and in lung cancer, 27% vs. 67%, P = 0.001). The multivariable analysis confirmed the prognostic value of ActA independently of tumour stage or inflammatory markers, particularly in lung cancer. Low muscularity was also an independent prognostic factor.ConclusionsOur study demonstrates that high ActA level is an independent prognosis factor of survival in cancer patients. More than a basic marker of the severity of the neoplastic disease or of the inflammatory process, ActA seems to influence survival by contributing to the development of cachexia and loss of skeletal muscle mass.

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Section: Resultsmentioning

confidence: 99%

Circulating Activin A predicts survival in cancer patients

Loumaye

Barsy

Nachit

et al. 2017

J cachexia sarcopenia muscle

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“…A number of factors have been discovered that antagonize myostatin activity, such as follistatin (24), recently suggested to induce muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin (41). However, the direct relevance of myostatin for satellite cells is still debated, and controversial models have been proposed regarding which cell types mediate the effects of myostatin on muscle physiology (41,43).…”

Section: Discussionmentioning

confidence: 99%

Cripto regulates skeletal muscle regeneration and modulates satellite cell determination by antagonizing myostatin

Guardiola

Lafuste

Brunelli

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Skeletal muscle regeneration mainly depends on satellite cells, a population of resident muscle stem cells. However, our understanding of the molecular mechanisms underlying satellite cell activation is still largely undefined. Here, we show that Cripto, a regulator of early embryogenesis, is a novel regulator of muscle regeneration and satellite cell progression toward the myogenic lineage. Conditional inactivation of cripto in adult satellite cells compromises skeletal muscle regeneration, whereas gain of function of Cripto accelerates regeneration, leading to muscle hypertrophy. Moreover, we provide evidence that Cripto modulates myogenic cell determination and promotes proliferation by antagonizing the TGF-β ligand myostatin. Our data provide unique insights into the molecular and cellular basis of Cripto activity in skeletal muscle regeneration and raise previously undescribed implications for stem cell biology and regenerative medicine. myogenic commitment | skeletal muscle stem cells | teratocarcinoma derived growth factor-1 (TDGF-1) | growth differentiation factor-8 (GDF-8)

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“…2004; Gilson et al. 2009), each inhibiting its biological function. Myostatin has both paracrine and endocrine effects (Zimmers et al.…”

Section: Introductionmentioning

confidence: 99%

Lifelong exercise, but not short-term high-intensity interval training, increases GDF11, a marker of successful aging: a preliminary investigation

et al. 2017

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Lifelong exercise is associated with regulation of skeletal mass and function, reductions in frailty, and successful aging. Yet, the influence of exercise on myostatin and myostatin‐interacting factors is relatively under examined in older males. Therefore, we investigated whether serum total myostatin, free myostatin, follistatin, and growth and differentiation factor 11 (GDF11) were altered following high‐intensity interval training (HIIT) in a group of 13 lifelong sedentary (SED; 64 [6] years) and 11 lifelong exercising (LEX; 62 [6] years) older males. SED follistatin was moderately greater than LEX pre‐HIIT (Cohen's d = 0.66), and was largely greater post‐HIIT (Cohen's d = 1.22). The HIIT‐induced increase in follistatin was large in SED (Cohen's d = 0.82) and absent in LEX (Cohen's d = 0.03). GDF11 was higher in LEX pre‐HIIT (Cohen's d = 0.49) and post‐HIIT (Cohen's d = 0.63) compared to SED. HIIT resulted in no change to GDF11 in LEX or SED (Cohen's d = 0.00–0.03). Peak power output and GDF11 were correlated (r = 0.603), independent of grouping. Differences in GDF11 with lifelong exercise training, paired with the correlation between GDF11 and peak power output, suggested that GDF11 may be a relevant myostatin‐interacting peptide to successful aging in humans, and strategies to maintain this need to be further explored.

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Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin

Cited by 211 publications

References 48 publications

Circulating Activin A predicts survival in cancer patients

Circulating Activin A predicts survival in cancer patients

Cripto regulates skeletal muscle regeneration and modulates satellite cell determination by antagonizing myostatin

Lifelong exercise, but not short-term high-intensity interval training, increases GDF11, a marker of successful aging: a preliminary investigation

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