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Adipose tissue-specific Nrf2 knockdown inhibits the cGAS-STING pathway to attenuate inflammation in obese mice

Lin Zhao1, Lina Tuerxunaili1, Guiyun Shi1

  • 1State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Key Laboratory of Molecular Biology for Endemic Diseases, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi, China.

Frontiers in Endocrinology
|January 28, 2026
PubMed
Abstract

Insights

Targeting adipose tissue-specific Nuclear factor erythroid 2-related factor 2 (NRF2) knockdown can reduce obesity and inflammation. This approach inhibits the cGAS-STING pathway, offering a new therapeutic strategy for metabolic disorders.

Area of Science:

  • Metabolic disorders
  • Obesity research
  • Inflammation and immunity

Background:

  • Obesity is a chronic inflammatory disease linked to oxidative stress and adipose tissue expansion.
  • Nuclear factor erythroid 2-related factor 2 (NRF2) is a key antioxidant factor in adipose tissue, interacting with the cGAS-STING pathway.
  • The roles of NRF2 and the cGAS-STING pathway in obesity-related metabolic dysfunction require further investigation.

Purpose of the Study:

  • To investigate the impact of adipose tissue-specific Nrf2 knockout (Nrf2Δ/adipo) on obesity-related metabolic phenotypes and inflammation in mice.
  • To elucidate the underlying mechanisms by which Nrf2 influences obesity and metabolic health.

Main Methods:

  • Generation of an Nrf2Δ/adipo mouse model and induction of obesity via high-fat diet (HFD).
  • Assessment of metabolic parameters including body weight, fat mass, glucose tolerance, and insulin sensitivity.
  • Utilized RNA sequencing, western blotting, flow cytometry, and ELISA to analyze gene/protein expression, inflammatory markers, and cellular changes.

Main Results:

  • Nrf2Δ/adipo mice showed reduced body weight, fat mass, triglycerides, and cholesterol, with improved glucose and insulin tolerance compared to controls.
  • These mice exhibited increased energy expenditure and reduced adipose tissue inflammation, including decreased M1 macrophages and proinflammatory factors.
  • Knockdown of Nrf2 in adipose tissue downregulated the cGAS-STING pathway, decreased inflammatory markers, and altered mitochondrial function.

Conclusions:

  • Adipose tissue-specific Nrf2 knockdown attenuates obesity-induced inflammation by inhibiting the cGAS-STING pathway.
  • This study identifies a novel therapeutic target within the adipose-specific antioxidant-inflammatory regulatory network for treating obesity-related metabolic disorders.
Keywords:
Nrf2adipose tissuecGAS-STINGhigh-fat dietinflammationobesityoxidative stress

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