Mitochondrial quality control at the ferroptosis-pyroptosis interface in diabetic cardiomyopathy: a narrative critical synthesis
- 1Heilongjiang University of Chinese Medicine, Harbin, China
- 2Department of Endocrinology II, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin, China
Abstract
Diabetic cardiomyopathy is clinically heterogeneous, whereas much of its mechanistic literature relies on experimental models. This narrative critical synthesis examines whether mitochondrial quality control links diabetic stress to ferroptosis, pyroptosis, and multicellular remodeling. The evidence base is an author-selected set of 112 publications mapped from a 400-record collection, supplemented by methodological and clinical context. Original database-specific search histories were not retained in the available materials. PubMed Central full text was available for 66 corpus records; 46 were initially accessible only as abstracts. A focused full-text reassessment of selected original reports replaces the earlier corpus-wide support labels. We distinguish core quality-control processes from associated metabolic regulators and separate death markers from functional evidence of execution. The best-supported findings concern model-specific changes in mitochondrial function, lipid-peroxide-sensitive injury, and intercellular communication. They do not establish a universal mitochondrial quality-control hierarchy or same-cell ferroptosis-pyroptosis co-execution. No single study identified in the available evidence demonstrates all three transitions from markers to execution, from one death program to another, and from rodents to a corresponding human mechanism. We compare same-cell coupling with cross-cell propagation and specify experiments that would distinguish them. Human phenotype and prognosis associations support disease relevance but cannot establish myocardial death mechanisms or therapeutic mediation. The resulting framework treats mitochondrial quality control as interacting, separable processes that may alter susceptibility to particular death programs, rather than as an established master regulator.
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BibTeX
@article{sun2026mitochondrial,
title = {{Mitochondrial quality control at the ferroptosis-pyroptosis interface in diabetic cardiomyopathy: a narrative critical synthesis}},
author = {Shibo Sun and Jiarui Li and Mingxiu Sun and Xin Song and Ming Tang and Likun Du},
journal = {Frontiers in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.3389/fcvm.2026.1950950},
url = {https://doi.org/10.3389/fcvm.2026.1950950},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Mitochondrial quality control at the ferroptosis-pyroptosis interface in diabetic cardiomyopathy: a narrative critical synthesis
AU - Shibo Sun
AU - Jiarui Li
AU - Mingxiu Sun
AU - Xin Song
AU - Ming Tang
AU - Likun Du
PY - 2026
DA - 2026/10/12
JO - Frontiers in Cardiovascular Medicine
DO - 10.3389/fcvm.2026.1950950
UR - https://doi.org/10.3389/fcvm.2026.1950950
AB - Diabetic cardiomyopathy is clinically heterogeneous, whereas much of its mechanistic literature relies on experimental models. This narrative critical synthesis examines whether mitochondrial quality control links diabetic stress to ferroptosis, pyroptosis, and multicellular remodeling. The evidence base is an author-selected set of 112 publications mapped from a 400-record collection, supplemented by methodological and clinical context. Original database-specific search histories were not retained in the available materials. PubMed Central full text was available for 66 corpus records; 46 were initially accessible only as abstracts. A focused full-text reassessment of selected original reports replaces the earlier corpus-wide support labels. We distinguish core quality-control processes from associated metabolic regulators and separate death markers from functional evidence of execution. The best-supported findings concern model-specific changes in mitochondrial function, lipid-peroxide-sensitive injury, and intercellular communication. They do not establish a universal mitochondrial quality-control hierarchy or same-cell ferroptosis-pyroptosis co-execution. No single study identified in the available evidence demonstrates all three transitions from markers to execution, from one death program to another, and from rodents to a corresponding human mechanism. We compare same-cell coupling with cross-cell propagation and specify experiments that would distinguish them. Human phenotype and prognosis associations support disease relevance but cannot establish myocardial death mechanisms or therapeutic mediation. The resulting framework treats mitochondrial quality control as interacting, separable processes that may alter susceptibility to particular death programs, rather than as an established master regulator.
SN - 2297-055X
ER -