scispace - formally typeset
C

Christopher L. Mendias

Researcher at Hospital for Special Surgery

Publications -  113
Citations -  4624

Christopher L. Mendias is an academic researcher from Hospital for Special Surgery. The author has contributed to research in topics: Skeletal muscle & Tendon. The author has an hindex of 35, co-authored 109 publications receiving 3541 citations. Previous affiliations of Christopher L. Mendias include University of Arizona & Cornell University.

Papers
More filters
Journal ArticleDOI

Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia.

TL;DR: It is suggested that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis.
Journal ArticleDOI

Atrogin-1, MuRF-1, and sarcopenia.

TL;DR: This review discusses aging-related changes to skeletal muscle structure and function; the regulation of protein synthesis and protein degradation by IGF-1, TGF-β, and myostatin; and the potential for modulating atrogin-1 and MuRF-1 expression to treat or prevent sarcopenia.
Journal ArticleDOI

Musculoskeletal Consequences of COVID-19.

TL;DR: The purpose of this article was to summarize the known musculoskeletal pathologies in patients with SARS or COVID-19 and to combine this with computational modeling and biochemical signaling studies to predict musculOSkeletal cellular targets and long-term consequences of the SARS-CoV-2 infection.
Journal ArticleDOI

Bigger Muscles and Smaller Tendons - Tendons of Myostatin Deficient Mice are Small, Brittle, and Hypocellular

TL;DR: It is concluded that, in addition to the regulation of muscle mass and force, myostatin regulates the structure and function of tendon tissues.
Journal ArticleDOI

Tendons of myostatin-deficient mice are small, brittle, and hypocellular.

TL;DR: In this paper, myostatin-null mice (MSTN−/−) were smaller and had a decrease in fibroblast density and decreased expression of type I collagen, scleraxis and tenomodulin.