• 国家药监局综合司 国家卫生健康委办公厅
  • 国家药监局综合司 国家卫生健康委办公厅

Research Progress on Mechanism of Nrf2-Mediated Mitophagy in Heart Failure and Intervention with Traditional Chinese Medicine

Corresponding author: LIN Lin, 1276302825@qq.com
DOI: 10.12201/bmr.202606.00080
Statement: This article is a preprint and has not been peer-reviewed. It reports new research that has yet to be evaluated and so should not be used to guide clinical practice.
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    Abstract: Heart failure (HF) represents the end-stage of various cardiovascular diseases, whose pathogenesis involves multiple pathological processes including oxidative stress and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2) acts as a core regulator of oxidative stress in the organism, while mitochondrial autophagy (MA) serves as a key mechanism maintaining the stability of mitochondrial quality and function in cardiomyocytes.Accumulating evidence in recent years has demonstrated that the Nrf2-mediated MA pathway is of great significance for delaying HF progression. This paper elaborates on the structures and biological functions of Nrf2 and MA, explores the molecular pathways underlying the involvement of Nrf2-mediated MA in the pathological progression of HF, and summarizes research advances in traditional Chinese medicine (TCM) interventions for HF targeting this pathway, so as to provide theoretical support for elucidating HF pathological mechanisms and developing novel strategies for its clinical prevention and treatment.

    Key words: Heart Failure; Nuclear Factor Erythroid 2-Related Factor 2; Mitochondrial Autophagy

    Submit time: 29 June 2026

    Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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  • ID Submit time Number Download
    1 2026-05-14

    10.12201/bmr.202606.00080V1

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喻鑫荣, LIN Lin, QUAN Yuting. Research Progress on Mechanism of Nrf2-Mediated Mitophagy in Heart Failure and Intervention with Traditional Chinese Medicine. 2026. biomedRxiv.202606.00080

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