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Irisin maintains ER homeostasis and activates AMPK via integrin αVβ5 to attenuate CSE + LPS-induced emphysema and inflammation
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DOI：10.1186/s12931-026-03850-9.png)
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Abstract
En 中文
AECOPD adversely affects patient survival rates and overall quality of life. Irisin is being increasingly recognized for its therapeutic potential in attenuating pulmonary injury, but its underlying mechanism remains unclear. Human lung tissue samples were subjected to IHC analysis for irisin, integrin αVβ5, and GRP78 expression. CSE+LPS-induced mouse and cell models were used to investigate whether irisin protects against emphysema and inflammation by regulating ER homeostasis and AMPK activity via integrin αVβ5. In COPD patients, irisin levels are decreased, whereas integrin αVβ5 and GRP78 levels are elevated. Irisin improved lung function and attenuated emphysema and inflammation in mice, and these effects were abolished by cilengitide. Irisin directly bound to integrin αVβ5, maintained ER homeostasis via the PERK/ATF4/CHOP pathway, and activated AMPK. These protective effects were lost upon integrin αVβ5 knockdown. These findings suggest that through integrin αVβ5, irisin concurrently maintains ER homeostasis and activates AMPK, thereby alleviating CSE+LPS-induced emphysema and inflammation, suggesting a novel therapeutic direction for the management of AECOPD.
Keywords:
Irisin
Integrin αVβ5
ER stress
AMPK
Emphysema
Inflammation
Journal
IF:
5
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803
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1.5W
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Cited Papers