Cai L, Tan Y, Islam MS, Horowitz M, Wintergerst KA. Diabetic cardiomyopathy: Importance of direct evidence to support the roles of NOD-like receptor protein 3 inflammasome and pyroptosis. World J Diabetes 2024; 15(8): 1659-1662 [PMID: 39192865 DOI: 10.4239/wjd.v15.i8.1659]
Corresponding Author of This Article
Lu Cai, MD, PhD, Professor, Pediatric Research Institute, Departments of Pediatrics, Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Wendy Novak Diabetes Institute, Norton Children’s Hospital, 570 S. Preston Street, Baxter I, Rm: 304F, Louisville, KY 40202, United States. lu.cai@louisville.edu
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Aug 15, 2024; 15(8): 1659-1662 Published online Aug 15, 2024. doi: 10.4239/wjd.v15.i8.1659
Diabetic cardiomyopathy: Importance of direct evidence to support the roles of NOD-like receptor protein 3 inflammasome and pyroptosis
Lu Cai, Yi Tan, Md Shahidul Islam, Michael Horowitz, Kupper A Wintergerst
Lu Cai, Yi Tan, Pediatric Research Institute, Departments of Pediatrics, Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Wendy Novak Diabetes Institute, Norton Children’s Hospital, Louisville, KY 40202, United States
Md Shahidul Islam, Department of Biochemistry, School of Life Sciences, University of KwaZulu-Natal, Durban 4000, KwaZulu-Natal, South Africa
Michael Horowitz, Department of Medicine, University of Adelaide, Adelaide 5005, Australia
Kupper A Wintergerst, Pediatric Research Institute, Division of Endocrinology, Department of Pediatrics, Wendy Novak Diabetes Institute, Norton Children’s Hospital, University of Louisville, Louisville, KY 40202, United States
Author contributions: Cai L, Tan Yi, and Wintergerst K conceptualized and drafted the first draft of the editorial; Islam MS and Horowitz M did further revisions and editorial corrections before submission.
Conflict-of-interest statement: The authors have no conflict of interest within this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Lu Cai, MD, PhD, Professor, Pediatric Research Institute, Departments of Pediatrics, Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Wendy Novak Diabetes Institute, Norton Children’s Hospital, 570 S. Preston Street, Baxter I, Rm: 304F, Louisville, KY 40202, United States. lu.cai@louisville.edu
Received: March 15, 2024 Revised: May 26, 2024 Accepted: June 6, 2024 Published online: August 15, 2024 Processing time: 132 Days and 11.7 Hours
Core Tip
Core Tip: The involvement of the NOD-like receptor protein 3 (NLRP3) inflammasome and pyroptosis in the pathogenesis of diabetic cardiomyopathy (DCM) has been extensively explored. However, most studies focused on whether diabetes causes NLRP3 inflammasome activation and pyroptosis in the diabetic heart, as well as the potential of medications and natural products to mitigate DCM progression along with reducing NLRP3 inflammasome expression and pyroptosis. Few studies directly investigated the roles of NLRP3 inflammasome and pyroptosis in the development of DCM, utilizing appropriate approaches, such as NLRP3 gene silencing or pharmaceutical NLRP3 inhibitors. Therefore, this aspect of investigation is an urgent need, as stated in this editorial.
