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Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies
Yuyuan Lu1, Jia Cui1, Xueyan Cheng1
1School of Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, Gansu Province, China.
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.
Insights
Diabetic cardiomyopathy involves regulated cell death and inflammation, damaging heart function. Targeting these interconnected pathways offers potential new treatments for this diabetes complication.
Area of Science:
- Cardiology
- Pathophysiology
- Molecular Biology
Background:
- Diabetic cardiomyopathy (DCM) is a significant diabetes complication, marked by heart dysfunction, fibrosis, and injury.
- The underlying mechanisms of DCM are not fully understood, limiting effective therapeutic interventions.
- Emerging evidence implicates regulated cell death (RCD) and inflammation in DCM pathogenesis.
Purpose of the Study:
- To review the intricate interplay between RCD and inflammatory signaling in DCM.
- To elucidate the contribution of these pathways to myocardial damage and fibrosis.
- To explore potential therapeutic strategies targeting both RCD and inflammation for DCM.
Main Methods:
- Literature review focusing on RCD pathways (apoptosis, pyroptosis, ferroptosis, necroptosis).
- Analysis of inflammatory signaling cascades (NLRP3, NF-κB, TLR4) and associated cytokines.
- Examination of the feedback loop between RCD and inflammation in the context of DCM.
Main Results:
- RCD is a key driver of myocardial injury in DCM, often linked to oxidative stress.
- Inflammatory pathways activate pro-fibrotic and pro-apoptotic signaling, worsening heart failure.
- A positive feedback loop exists where RCD and inflammation mutually amplify, accelerating DCM progression.
Conclusions:
- RCD and inflammation are critical, interconnected players in diabetic cardiomyopathy.
- Targeting both RCD and inflammatory pathways simultaneously presents a promising therapeutic avenue.
- A multi-targeted approach may provide novel treatment strategies for DCM.
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