Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype.
A, L., G, M., G, P., F, C., S, S., J, C., F, B., M, A., F, C., & C, C. (2026). Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype.. Cells. https://doi.org/10.3390/cells15121131
A L, G M, G P, F C, S S, J C, et al. Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype.. Cells. 2026; doi: 10.3390/cells15121131
A L, G M, G P, et al. Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype.[J]. Cells. 2026. DOI: 10.3390/cells15121131.
@article{a2026,
author = {Lattanzio A and Marchionni G and Pecci G and Ciccarelli F and Stavagna S and Costantino J and Ballatore F and Alfarano M and Ciciarello F and Chimenti C},
title = {Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype.},
journal = {Cells},
year = {2026},
doi = {10.3390/cells15121131},
note = {PMID: 42346158},
}
TY - JOUR AU - Lattanzio A AU - Marchionni G AU - Pecci G AU - Ciccarelli F AU - Stavagna S AU - Costantino J AU - Ballatore F AU - Alfarano M AU - Ciciarello F AU - Chimenti C TI - Inflammation in Cardiomyopathies: Cellular Mechanisms Across Cardiac Phenotype. T2 - Cells PY - 2026 DO - 10.3390/cells15121131 AN - PMID:42346158 ER -
Cardiomyopathies are traditionally classified by structural and genetic phenotypes, but emerging evidence highlights chronic myocardial inflammation as a pivotal driver of disease progression across different etiologies. This review synthesizes the current literature on the cellular and molecular inflammatory mechanisms underlying hypertrophic cardiomyopathy, Anderson-Fabry disease, cardiac amyloidosis, arrhythmogenic cardiomyopathy, and dilated cardiomyopathy. Across these distinct conditions, endogenous triggers such as metabolic substrates, misfolded amyloid fibrils, mechanical stress, or viral genomes act as damage-associated molecular patterns. These stimuli activate innate and adaptive immune cascades, notably the Toll-like receptors, the NF-κB pathway, and the NLRP3 inflammasome. This immune activation establishes a pro-inflammatory microenvironment that promotes fibroblast reprogramming, myocardial edema, and progressive fibrotic or fibro-fatty remodeling. Inflammation is an active, core pathophysiological mechanism rather than a passive secondary bystander in cardiomyopathies. Recognizing these shared immune pathways provides a framework for improved risk stratification and highlights the potential for targeted immunomodulatory therapies to alter disease trajectories.