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Autophagy, Apr 07 2025, | https://doi.org/10.1080/15548627.2025.2487035
BNIP3-mediated mitophagy in macrophages regulates obesity-induced adipose tissue metaflammation
Sangseob Kim 1, Cheoljun Choi 1, Yeonho Son 1, Junhyuck Lee 1, Sungug Joo 1, Yun-Hee Lee 1 *
1College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
*Corresponding author: correspondence to Yun-Hee Lee
Abstract
Adipose tissue macrophages (ATMs) are key cellular components that respond to nutritional excess, contributing to obesity-induced inflammation and insulin resistance. However, the mechanisms underlying macrophage polarization and recruitment in adipose tissue during obesity remain unclear. In this study, we investigated mitophagy-dependent metabolic reprogramming in ATMs and identified a crucial role of the mitophagy receptor BNIP3 in regulating macrophage polarization in response to obesity. Mitophagic flux in ATMs increased following 12 weeks of high-fat diet (HFD) feeding, with Bnip3 levels upregulated in a HIF1A dependent manner, without affecting other mitophagy receptors. Macrophage-specific bnip3 knockout reduced HFD-induced adipose tissue inflammation and improved glucose tolerance and insulin sensitivity. Mechanistically, hypoxic conditions in vitro induced HIF1A-BNIP3-mediated mitophagy and glycolytic shift in macrophages. Furthermore, HIF1A-BNIP3 signaling-enhanced lipopolysaccharide-induced pro-inflammatory activation in macrophages. These findings demonstrate that BNIP3-mediated mitophagy regulates the glycolytic shift and pro-inflammatory polarization in macrophages and suggest that BNIP3 could be a therapeutical target for obesity-related metabolic diseases.
논문정보
- Research article
- 2025년 04월 (BRIC 등록일 2025-04-10)
- 국내 연구진
- 의약학 > 면역의학
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