HSF1 inhibits smooth muscle gene program to enhance white fat browning and hypermetabolism after burn injury.

Yankang Zhang, Yuhan Zheng, Bin Chen, Xinqian Li, Ting Zhang, Lingyan Xu, Jing Ma, Xinran Ma, Yu Li

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Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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9 authors.

Yankang Zhang *Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Yuhan Zheng *Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Bin Chen *Guangzhou Red Cross Hospital, Jinan University, Guangzhou, 510000, China.

Xinqian LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Ting ZhangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Lingyan XuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.

Jing MaDepartment of Endocrinology and Metabolism, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. majing@renji.com.

Xinran MaShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China. xrma@bio.ecnu.edu.cn.

Yu LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China. yli@bio.ecnu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe burn injury induces a prolonged hypermetabolic state that is associated with undesirable metabolic consequences. Heat shock factor 1 (HSF1) is the predominant transcription factor that responds to thermal stress and has been reported to orchestrate the browning gene program of subcutaneous white adipose tissue (sWAT), thereby promoting energy expenditure. However, the role of sWAT HSF1 in the pathogenesis of burn injury remains unclear. In this study, we report that burn injury notably upregulates the expression of HSF1 in sWAT. Moreover, the genetic ablation of HSF1 in adipose tissues attenuated the burn-induced sWAT browning and lipolysis, circulating lipid dysfunction, and liver injury. Conversely, specific overexpression of the active form of HSF1 in sWAT exacerbated these phenotypes. Notably, we found that burn injury largely suppressed sWAT smooth muscle-related gene programs and shifted toward browning gene programs. Mechanistically, HSF1, in cooperation with PRDM16, drives this phenotypic switch by directly inhibiting the expression of Myh11, which is the smooth muscle marker for sWAT reprogramming. Furthermore, the pharmacological inhibition of HSF1 with DTHIB ameliorated burn injury. Overall, these findings highlight that sWAT HSF1 is a key mediator of pathological hypermetabolism following severe burn injury.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteBurnsHeat Shock Transcription FactorsMuscle, SmoothAnimalsDNA-Binding ProteinsEnergy MetabolismGene Expression RegulationMaleMiceMice, Inbred C57BLMyosin Heavy ChainsTranscription FactorsDNA-Binding ProteinsHeat Shock Transcription FactorsHsf1 protein, mouseMyosin Heavy ChainsPrdm16 protein, mouseTranscription Factorsbrowningburn injuryHSF1hypermetabolismsmooth musclesWAT

Identifiers

PMID42132988

DOI10.1038/cddis.2016.22

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.