FABP3-mediated membrane lipid saturation alters fluidity and induces ER stress in skeletal muscle with aging

Cited 5 time in scopus
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Title
FABP3-mediated membrane lipid saturation alters fluidity and induces ER stress in skeletal muscle with aging
Author(s)
Seung-Min Lee; Seol Hee Lee; Y Jung; Y Lee; Jong Hyun Yoon; Jeong Yi Choi; Chae Young Hwang; Young Hoon Son; Sung Sup Park; G S Hwang; Kwang-Pyo LeeKi-Sun Kwon
Bibliographic Citation
Nature Communications, vol. 11, pp. 5661-5661
Publication Year
2020
Abstract
Sarcopenia is characterized by decreased skeletal muscle mass and function with age. Aged muscles have altered lipid compositions; however, the role and regulation of lipids are unknown. Here we report that FABP3 is upregulated in aged skeletal muscles, disrupting homeostasis via lipid remodeling. Lipidomic analyses reveal that FABP3 overexpression in young muscles alters the membrane lipid composition to that of aged muscle by decreasing polyunsaturated phospholipid acyl chains, while increasing sphingomyelin and lysophosphatidylcholine. FABP3-dependent membrane lipid remodeling causes ER stress via the PERK-eIF2α pathway and inhibits protein synthesis, limiting muscle recovery after immobilization. FABP3 knockdown induces a young-like lipid composition in aged muscles, reduces ER stress, and improves protein synthesis and muscle recovery. Further, FABP3 reduces membrane fluidity and knockdown increases fluidity in vitro, potentially causing ER stress. Therefore, FABP3 drives membrane lipid composition-mediated ER stress to regulate muscle homeostasis during aging and is a valuable target for sarcopenia.
ISSN
2041-1723
Publisher
Springer-Nature Pub Group
DOI
http://dx.doi.org/10.1038/s41467-020-19501-6
Type
Article
Appears in Collections:
Division of Research on National Challenges > Aging Research Center > 1. Journal Articles
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