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Review
. 2025 Oct 22.
doi: 10.1007/s12265-025-10701-3. Online ahead of print.

Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies

Yuyuan Lu  1 , Jia Cui  1 , Xueyan Cheng  1 , Jiawei Li  1 , Lingna Zhang  1 , Jiao Tian  1 , Ani Yang  2 , Lin Yi  3   4
Affiliations
Review

Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies

Yuyuan Lu et al. J Cardiovasc Transl Res. .

Abstract

Diabetic cardiomyopathy (DCM) is a common complication of diabetes, characterized by myocardial injury, fibrosis, and heart dysfunction. The pathogenesis remains poorly understood, with limited treatment options. Recent research highlights the roles of regulated cell death (RCD) and inflammation in DCM progression. RCD types, including apoptosis, pyroptosis, ferroptosis, and necroptosis, are central to myocardial damage and are closely linked to oxidative stress and inflammation. Inflammatory pathways like NLRP3, NF-κB, and TLR4 activate cytokines (TNF-α, IL-1β, IL-6), exacerbating fibrosis and heart failure. Notably, RCD and inflammation create a feedback loop, amplifying each other and accelerating DCM. This review explores the interactions between RCD and inflammatory signaling, their contribution to myocardial injury, and potential therapeutic strategies targeting both pathways. A multi-targeted approach to DCM therapy may offer new avenues for treatment.

Keywords: Cell death; Diabetic cardiomyopathy; Inflammatory signaling; Therapeutic strategies.

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Conflict of interest statement

Declarations. Ethics Approval: Not applicable, This piece of work is a review of prior publications. There was no collection or analysis of new data from human or animal participants in this research. Consent to Participate: Not applicable. Consent for Publication: The content of this manuscript is a compilation and analysis of pre-existing studies, and it is devoid of any individual data or images that necessitate consent for publication. Competing Interests: The authors declare that they have no conflict of interest.

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