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Role of pyroptosis in diabetic cardiomyopathy: an updated review. | LitMetric

Role of pyroptosis in diabetic cardiomyopathy: an updated review.

Front Endocrinol (Lausanne)

State Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Published: January 2024

AI Article Synopsis

  • * Pyroptosis, a type of programmed cell death linked to inflammation, has been found to worsen the progression of DCM, suggesting its role in the condition's development.
  • * The review summarizes mechanisms of how pyroptosis contributes to DCM and highlights potential treatments targeting the NLRP3 inflammasome, aiming to provide new insights for developing therapies for DCM.

Article Abstract

Diabetic cardiomyopathy (DCM), one of the common complications of diabetes, presents as a specific cardiomyopathy with anomalies in the structure and function of the heart. With the increasing prevalence of diabetes, DCM has a high morbidity and mortality worldwide. Recent studies have found that pyroptosis, as a programmed cell death accompanied by an inflammatory response, exacerbates the growth and genesis of DCM. These studies provide a theoretical basis for exploring the potential treatment of DCM. Therefore, this review aims to summarise the possible mechanisms by which pyroptosis promotes the development of DCM as well as the relevant studies targeting pyroptosis for the possible treatment of DCM, focusing on the molecular mechanisms of NLRP3 inflammasome-mediated pyroptosis, different cellular pyroptosis pathways associated with DCM, the effects of pyroptosis occurring in different cells on DCM, and the relevant drugs targeting NLRP3 inflammasome/pyroptosis for the treatment of DCM. This review might provide a fresh perspective and foundation for the development of therapeutic agents for DCM.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10796545PMC
http://dx.doi.org/10.3389/fendo.2023.1322907DOI Listing

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