Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 17, Pages -Publisher
MDPI
DOI: 10.3390/ijms231710008
Keywords
BAT-muscle cross talk; energy expenditure; Islr; muscle-derived IL-6; mitochondrial function; Ndufs2; thermogenesis
Funding
- National Key Research and Development Program of China [2021YFF1000603]
- National Natural Science Foundation of China [31790412, 31970712]
- Plan 111 [B12008]
- National Research Facility for Phenotypic and Genotypic Analysis of Model Animals (Beijing)
- earmarked fund for CARS36
Ask authors/readers for more resources
This study reveals a previously unrecognized mechanism for muscle-BAT crosstalk, involving Islr, Ndufs2, and IL-6, which play crucial roles in regulating energy homeostasis and may serve as potential therapeutic targets for obesity.
Brown adipose tissue (BAT) is functionally linked to skeletal muscle because both tissues originate from a common progenitor cell, but the precise mechanism controlling muscle-to-brown-fat communication is insufficiently understood. This report demonstrates that the immunoglobulin superfamily containing leucine-rich repeat (Islr), a marker of mesenchymal stromal/stem cells, is critical for the control of BAT mitochondrial function and whole-body energy homeostasis. The mice loss of Islr in BAT after cardiotoxin injury resulted in improved mitochondrial function, increased energy expenditure, and enhanced thermogenesis. Importantly, it was found that interleukin-6 (IL-6), as a myokine, participates in this process. Mechanistically, Islr interacts with NADH: Ubiquinone Oxidoreductase Core Subunit S2 (Ndufs2) to regulate IL-6 signaling; consequently, Islr functions as a brake that prevents IL-6 from promoting BAT activity. Together, these findings reveal a previously unrecognized mechanism for muscle-BAT cross talk driven by Islr, Ndufs2, and IL-6 to regulate energy homeostasis, which may be used as a potential therapeutic target in obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available