Imperial College London
Alternate

ProfessorNadiaRosenthal

Faculty of Medicine, National Heart & Lung Institute

Chair in Cardiovascular Science&ScientificDirector
 
 
 
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Contact

 

+44 (0)20 7594 2737n.rosenthal

 
 
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Location

 

424W2ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Ascenzi:2019:10.1111/acel.12954,
author = {Ascenzi, F and Barberi, L and Dobrowolny, G and Nova, Bacurau AV and Nicoletti, C and Rizzuto, E and Rosenthal, N and Scicchitano, BM and Musaro, A},
doi = {10.1111/acel.12954},
journal = {Aging Cell},
title = {Effects of IGF-1 isoforms on muscle growth and sarcopenia},
url = {http://dx.doi.org/10.1111/acel.12954},
volume = {18},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The decline in skeletal muscle mass and strength occurring in aging, referred as sarcopenia, is the result of many factors including an imbalance between protein synthesis and degradation, changes in metabolic/hormonal status, and in circulating levels of inflammatory mediators. Thus, factors that increase muscle mass and promote anabolic pathways might be of therapeutic benefit to counteract sarcopenia. Among these, the insulinlike growth factor1 (IGF1) has been implicated in many anabolic pathways in skeletal muscle. IGF1 exists in different isoforms that might exert different role in skeletal muscle. Here we study the effects of two full propeptides IGF1Ea and IGF1Eb in skeletal muscle, with the aim to define whether and through which mechanisms their overexpression impacts muscle aging. We report that only IGF1Ea expression promotes a pronounced hypertrophic phenotype in young mice, which is maintained in aged mice. Nevertheless, examination of aged transgenic mice revealed that the local expression of either IGF1Ea or IGF1Eb transgenes was protective against agerelated loss of muscle mass and force. At molecular level, both isoforms activate the autophagy/lysosome system, normally altered during aging, and increase PGC1α expression, modulating mitochondrial function, ROS detoxification, and the basal inflammatory state occurring at old age. Moreover, morphological integrity of neuromuscular junctions was maintained and preserved in both MLC/IGF1Ea and MLC/IGF1Eb mice during aging. These data suggest that IGF1 is a promising therapeutic agent in staving off advancing muscle weakness.
AU  - Ascenzi,F
AU  - Barberi,L
AU  - Dobrowolny,G
AU  - Nova,Bacurau AV
AU  - Nicoletti,C
AU  - Rizzuto,E
AU  - Rosenthal,N
AU  - Scicchitano,BM
AU  - Musaro,A
DO  - 10.1111/acel.12954
PY  - 2019///
SN  - 1474-9718
TI  - Effects of IGF-1 isoforms on muscle growth and sarcopenia
T2  - Aging Cell
UR  - http://dx.doi.org/10.1111/acel.12954
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000467861100021&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/74123
VL  - 18
ER  -
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