Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy-Reference-Cited by-同舟云学术

Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy

Published:2024-01-01 Issue:1 Volume:326 Page:E50-E60
ISSN:0193-1849
Container-title:American Journal of Physiology-Endocrinology and Metabolism
language:en
Short-container-title:American Journal of Physiology-Endocrinology and Metabolism

Author:

Petrocelli Jonathan J.¹,Liu Jingtong²,Yee Elena M.³,Ferrara Patrick J.⁴,Bourrant Paul-Emile³,de Hart Naomi M. M. P.³,Tatum Sean M.³^ORCID,Holland William J.³⁴,Funai Katsuhiko³⁴^ORCID,Drummond Micah J.¹³⁴^ORCID

Affiliation:

1. Department of Physical Therapy and Athletic Training, University of Utah, Salt Lake City, Utah, United States

2. Spencer Fox Eccles School of Medicine, University of Utah, Salt Lake City, Utah, United States

3. Department of Nutrition & Integrative Physiology, University of Utah, Salt Lake City, Utah, United States

4. Molecular Medicine Program, University of Utah, Salt Lake City, Utah, United States

Abstract

We determined that skeletal muscle-specific AMPKα knockout (KO) mice display functional, fibrotic, and transcriptional alterations before and during muscle disuse atrophy. We also observed that AMPKα KO drives muscle fibrosis and pathways related to cellular senescence that continues during the hindlimb unloading period.

Funder

HHS | NIH | National Institute on Aging

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpendo.00261.2023

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