Insight into Cardiomyopathy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 15065

Special Issue Editor


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Guest Editor
Department of Pharmacology & System Physiology, Cardiovascular Research Center, University of Cincinnati, 3230 Eden Ave, Cincinnati, OH 45267, USA
Interests: heart failure; metabolism; cardiac hypertrophy; diabetic cardiomyopathy

Special Issue Information

Dear Colleagues,

Cardiomyopathy, a pervasive heart muscle disease, has emerged as a leading cause of global mortality, with its incidence doubling over the past century. Cardiomyopathy causes weakness of the heart muscle, which makes it harder for the heart to pump blood effectively. Over time, this can lead to heart failure, arrhythmias (irregular heartbeats), and other complications. The pressing need for effective treatments necessitates a profound understanding of cardiomyopathy at the cellular and molecular levels to discover molecules that can be translated into innovative medicines. 

This Special Issue will cover a range of topics, including advancements in in vitro and in vivo models for studying cardiomyopathy, insights into the mechanisms of cardiac remodeling myopathy in animal models, and the identification of key cellular and molecular targets to accelerate the translation of groundbreaking discoveries into tangible medical solutions, ultimately improving outcomes for those affected by this life-threatening condition.

Dr. Sobuj Mia
Guest Editor

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Keywords

  • heart failure
  • ventricular dysfunction
  • hypertrophic cardiomyopathy
  • dilated cardiomyopathy
  • cardiac fibrosis
  • cardiac hypertrophy
  • biomarkers

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Published Papers (1 paper)

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Research

13 pages, 5202 KiB  
Article
Spike Protein of SARS-CoV-2 Activates Cardiac Fibrogenesis through NLRP3 Inflammasomes and NF-κB Signaling
by Huynh Van Tin, Lekha Rethi, Satoshi Higa, Yu-Hsun Kao and Yi-Jen Chen
Cells 2024, 13(16), 1331; https://doi.org/10.3390/cells13161331 - 11 Aug 2024
Cited by 2 | Viewed by 13937
Abstract
Background: The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is crucial to viral entry and can cause cardiac injuries. Toll-like receptor 4 (TLR4) and NOD-, LPR-, and pyrin-domain-containing 3 (NLRP3) inflammasome are critical immune system components implicated in cardiac fibrosis. [...] Read more.
Background: The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is crucial to viral entry and can cause cardiac injuries. Toll-like receptor 4 (TLR4) and NOD-, LPR-, and pyrin-domain-containing 3 (NLRP3) inflammasome are critical immune system components implicated in cardiac fibrosis. The spike protein activates NLRP3 inflammasome through TLR4 or angiotensin-converting enzyme 2 (ACE2) receptors, damaging various organs. However, the role of spike protein in cardiac fibrosis in humans, as well as its interactions with NLRP3 inflammasomes and TLR4, remain poorly understood. Methods: We utilized scratch assays, Western blotting, and immunofluorescence to evaluate the migration, fibrosis signaling, mitochondrial calcium levels, reactive oxygen species (ROS) production, and cell morphology of cultured human cardiac fibroblasts (CFs) treated with spike (S1) protein for 24 h with or without an anti-ACE2 neutralizing antibody, a TLR4 blocker, or an NLRP3 inhibitor. Results: S1 protein enhanced CFs migration and the expressions of collagen 1, α-smooth muscle actin, transforming growth factor β1 (TGF-β1), phosphorylated SMAD2/3, interleukin 1β (IL-1β), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). S1 protein increased ROS production but did not affect mitochondrial calcium content and cell morphology. Treatment with an anti-ACE2 neutralizing antibody attenuated the effects of S1 protein on collagen 1 and TGF-β1 expressions. Moreover, NLRP3 (MCC950) and NF-kB inhibitors, but not the TLR4 inhibitor TAK-242, prevented the S1 protein-enhanced CFs migration and overexpression of collagen 1, TGF-β1, and IL-1β. Conclusion: S1 protein activates human CFs by priming NLRP3 inflammasomes through NF-κB signaling in an ACE2-dependent manner. Full article
(This article belongs to the Special Issue Insight into Cardiomyopathy)
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