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Cells
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Insight into Cardiomyopathy
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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: closed (20 March 2026) | Viewed by 22385

Editor

Dr. Sobuj Mia

E-Mail Website
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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (3 papers)

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Research

13 pages, 2578 KB  
Article
Administration of Nicotinamide Mononucleotide Mitigates the HIV Nef-Induced Metabolic and Pathological Changes in the Heart
by Olena Kondrachuk, Esther Nakhungu, Gbenga Ogundipe, Nishit Tailor, Pierce Ciccone, Kim Hong, Anvita Gadiraju, Yuka Kimura, Artemis Zi, Sumaya Yusuf, Aya Alkousa, Sarah Nguyen, Rithvik Rajkumar, Jaycee Do, Jay Rappaport and Manish Kumar Gupta
Cells 2026, 15(5), 444; https://doi.org/10.3390/cells15050444 - 1 Mar 2026
Cited by 1 | Viewed by 1190
Abstract
Due to the application of antiretroviral therapy, HIV has become a manageable chronic disease, and people living with HIV/AIDS (PLWHA) experience several comorbidities, including cardiovascular disease. Although antiretroviral therapy suppresses the viral load to an undetectable level, HIV proteins can still be detected [...] Read more.
Due to the application of antiretroviral therapy, HIV has become a manageable chronic disease, and people living with HIV/AIDS (PLWHA) experience several comorbidities, including cardiovascular disease. Although antiretroviral therapy suppresses the viral load to an undetectable level, HIV proteins can still be detected in the circulation and in different organs. In our previous study, we found that the expression of the Nef protein causes cardiac dysfunction and heart failure in a transgenic mouse model. We also observed inhibition of autophagy along with the upregulation of the senescence marker Bcl2. To further understand the metabolic changes related to Nef in cardiac tissue, we examined nicotinamide adenine dinucleotide (NAD) metabolism in the heart. Our metabolic study with cardiac tissue revealed that Nef expression decreases NAD+ levels in the heart. Additionally, we explored whether replenishing cellular NAD+ could be a potential therapeutic target for HIV-associated cardiovascular disease. Interestingly, our study found that NMN treatment can improve cellular autophagy, decrease the senescence marker Bcl2, and reduce fibrosis in the heart. Overall, our study suggests that NMN could serve as a promising therapeutic molecule for the treatment of HIV-associated cardiovascular comorbidities. Full article
(This article belongs to the Special Issue Insight into Cardiomyopathy)
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21 pages, 4907 KB  
Article
Atrial TRPM2 Channel-Mediated Ca2+ Influx Regulates ANP Secretion and Protects Against Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis
by Tomohiro Numata, Hideaki Tagashira, Kaori Sato-Numata, Meredith C Hermosura, Fumiha Abe, Ayako Sakai, Shinichiro Yamamoto and Hiroyuki Watanabe
Cells 2026, 15(1), 24; https://doi.org/10.3390/cells15010024 - 22 Dec 2025
Cited by 3 | Viewed by 1399
Abstract
Transient receptor potential melastatin 2 (TRPM2) channel is a Ca2+-permeable, redox-activated cardiac ion channel protective in ischemia–reperfusion, but whether it regulates atrial endocrine output under stress is unclear. Here, we investigated whether TRPM2 contributes to the atrial natriuretic peptide (ANP) response [...] Read more.
Transient receptor potential melastatin 2 (TRPM2) channel is a Ca2+-permeable, redox-activated cardiac ion channel protective in ischemia–reperfusion, but whether it regulates atrial endocrine output under stress is unclear. Here, we investigated whether TRPM2 contributes to the atrial natriuretic peptide (ANP) response during β-adrenergic stimulation. We compared how male C57BL/6J wild-type (WT) and TRPM2 knockout (TRPM2−/−) mice (8–12 weeks old) respond to β-adrenergic stress induced by isoproterenol (ISO) using echocardiography, histology, RT-PCR, electrophysiology, Ca2+ imaging, ELISA, and atrial RNA-seq. We detected abundant Trpm2 transcripts in WT atria and measured ADP-ribose (ADPr)-evoked currents and hydrogen peroxide (H2O2)-induced Ca2+ influx characteristic of TRPM2; these were absent in TRPM2−/− cells. Under the ISO-induced hypertrophic model, TRPM2−/− mice developed greater cardiac hypertrophy, fibrosis, and systolic dysfunction compared with WT mice. Atrial bulk RNA-seq showed significant induction of Nppa (ANP precursor gene) in WT + ISO, accompanied by higher circulating ANP; TRPM2−/− + ISO showed blunted Nppa and ANP responses. ISO-treated TRPM2−/− mice exhibited more blunt responses, in both Nppa transcripts and circulating ANP levels. Exogenous ANP attenuated ISO-induced dysfunction, hypertrophy, and fibrosis in TRPM2−/− mice, suggesting that TRPM2 is needed for the cardioprotective endocrine response via ANP to control stress-induced β-adrenergic remodeling. Full article
(This article belongs to the Special Issue Insight into Cardiomyopathy)
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13 pages, 5202 KB  
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 15 | Viewed by 18024
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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