Molecular and Cellular Mechanisms of Heart Disease

Topic Information

Dear Colleagues,

Heart failure is still a leading cause of mortality worldwide. Cardiomyocytes contribute to heart failure by losing the ability to generate sufficient force to pump blood into circulation. To improve the current treatment options in cardiology, it is important to have a better understanding of the biological behavior of cardiomyocytes. The function of these cells cannot be completely understood independently of the interaction with surrounding cells, i.e., cardiac fibroblasts and vascular cells. Nevertheless, cardiomyocytes are the cells that must generate heart work. They can modify parts of their electromechanical coupling machinery, electrometabolic coupling, or increase in size via hypertrophy. However, hypertrophy can be either adaptive or maladaptive, and the transition from the one into the other type of hypertrophy is not clearly understood. Pathological hypertrophy is often characterised by cardiac fibrosis and contributes to cardiac dysfunction. Cell death, i.e., cardiomyocyte apoptosis, is another common feature of heart disease. Processes dealing with metabolism and mitochondrial function, electromechanical coupling, cell death, and electrophysiological aspects are among the processes that need to be addressed and understood in their molecular fine regulation in order to improve treatment regimes.

This Topic aims to summarize the current understanding of the process of developing heart failure with a focus on the force-generating cell, the cardiomyocyte.

Prof. Dr. Pasi Tavi
Prof. Dr. Ebru Arioglu-Inan
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	6.8	2013	21 Days	CHF 2600	Submit
Current Issues in Molecular Biology cimb	3.0	3.7	1999	16.3 Days	CHF 2200	Submit
International Journal of Molecular Sciences ijms	4.9	9.0	2000	17.8 Days	CHF 2900	Submit
Journal of Cardiovascular Development and Disease jcdd	2.3	3.7	2014	24.7 Days	CHF 2700	Submit
Organoids organoids	-	-	2022	27.8 Days	CHF 1200	Submit

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Published Papers (9 papers)

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26 pages, 18310 KB  

Open AccessArticle

Identification and Validation of MTFP1 as a Mitochondrial Target Restoring Dynamics and ECM Remodeling in Acute Myocardial Infarction

by Xi Hu, Hailong Bao, Yue Huang, Zhaoxing Cao, Wei Yang, Cheng Huang, Xin Chen, Yanbing Chen, Bingxiu Chen, Guiling Xia, Xiao Yang, Runze Huang and Zhangrong Chen

Curr. Issues Mol. Biol. 2026, 48(3), 293; https://doi.org/10.3390/cimb48030293 - 9 Mar 2026

Viewed by 409

Abstract

Background: Mitochondrial dysfunction is central to the pathogenesis of acute myocardial infarction (AMI), but mitochondria-related molecular biomarkers and mechanisms remain incompletely defined. This study aimed to identify mitochondria-associated biomarkers in AMI and elucidate their functional roles in mitochondrial dynamics, extracellular matrix (ECM) [...] Read more.

Background: Mitochondrial dysfunction is central to the pathogenesis of acute myocardial infarction (AMI), but mitochondria-related molecular biomarkers and mechanisms remain incompletely defined. This study aimed to identify mitochondria-associated biomarkers in AMI and elucidate their functional roles in mitochondrial dynamics, extracellular matrix (ECM) remodeling, and cardiac protection. Methods: Two GEO datasets (GSE19322, GSE71906) were analyzed to identify mitochondria-related differentially expressed genes (DE-MRGs) by intersecting DEGs with MitoCarta3.0 genes. Functional enrichment (GO/KEGG), LASSO regression, ROC curves, and nomogram modeling were employed to screen biomarkers. Immune infiltration profiling, GeneMANIA, GSEA, TF-mRNA and ceRNA network construction, and drug prediction analyses were performed. Expression validation was conducted via RT-qPCR, Western blot (WB), and immunohistochemistry (IHC) in murine AMI models and hypoxia-induced cardiomyocytes. Functional assays assessed cardiac performance (echocardiography), infarct size (TTC staining), fibrosis (Masson/Sirius red), oxidative stress (ROS), and ECM remodeling (MMP9/TIMP1 axis). Results: We identified 295 DE-MRGs, enriched in oxidative phosphorylation and mitochondrial metabolic pathways. Machine learning and validation analyses pinpointed MTFP1 and DNAJC28 as AMI biomarkers with strong diagnostic accuracy. In vivo and in vitro studies confirmed marked downregulation of MTFP1 post-AMI and under hypoxia. AAV9-mediated MTFP1 overexpression improved cardiac function, reduced infarct size, attenuated fibrosis, and decreased ROS levels. Mechanistically, MTFP1 upregulated phosphorylated DRP1 (Ser616) without altering total DRP1, balanced MMP9/TIMP1 activity, and suppressed fibrosis markers (COL1A1, α-SMA). Gelatin zymography indicated that MMP9 activation remained restrained despite elevated pro-MMP9, consistent with TIMP1-mediated regulation. Hypoxia-induced cardiomyocytes showed similar antifibrotic and antioxidative responses following MTFP1 overexpression. Conclusions: Our study identified MTFP1 as a novel mitochondria-related biomarker and therapeutic modulator in AMI. MTFP1 exerts cardioprotective effects by restoring mitochondrial fission balance and ECM remodeling through the p-DRP1/MMP9/TIMP1 signaling axis, attenuating fibrosis and oxidative stress. These findings provide mechanistic insight into mitochondria-targeted cardioprotection and highlight MTFP1 as a promising diagnostic and therapeutic target for AMI. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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19 pages, 2499 KB  

Open AccessArticle

First Glance at Myeloid Leukaemia Factor 2 in Cardiomyocytes

by Jakob Christoph Voran, Lucia Sophie Kilian, Simone Martini, Marcin Luzarowski, Marie Isabel Noormalal, Oliver Josef Müller, Ashraf Yusuf Rangrez and Derk Frank

J. Cardiovasc. Dev. Dis. 2026, 13(1), 19; https://doi.org/10.3390/jcdd13010019 - 30 Dec 2025

Viewed by 612

Abstract

Understanding the molecular mechanisms that maintain protein homeostasis in cardiomyocytes is fundamental for the development of causal therapies for heart failure. Chaperones, the ubiquitin–proteasome system and autophagy are major regulators of cardiac homeostasis and are crucial for cardiomyocyte function and survival. In this [...] Read more.

Understanding the molecular mechanisms that maintain protein homeostasis in cardiomyocytes is fundamental for the development of causal therapies for heart failure. Chaperones, the ubiquitin–proteasome system and autophagy are major regulators of cardiac homeostasis and are crucial for cardiomyocyte function and survival. In this context, myeloid leukaemia factor 2 (MLF2) emerged as a candidate of interest, as we found it overrepresented in protein aggregates in the hearts of mouse models of desmin-related cardiomyopathies (DRM), and it has also been suggested to be associated with dilated cardiomyopathy (DCM). Here, we identified αB-crystallin (CryAB), among other proteins, as a potential interaction partner of MLF2. Functionally, MLF2 was significantly upregulated in mouse models of heart failure and in two in vitro models of cardiomyocyte hypertrophy, and its overexpression resulted in attenuation of pro-hypertrophic gene expression. Taken together, these findings provide initial evidence supporting a role for MLF2 in regulating protein homeostasis and in modulating hypertrophic signalling in cardiomyocytes. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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15 pages, 1131 KB  

Open AccessReview

Mitochondrial Permeability Transition Pore: The Cardiovascular Disease’s Molecular Achilles Heel

by Salvatore Nesci and Speranza Rubattu

Biomedicines 2025, 13(12), 3014; https://doi.org/10.3390/biomedicines13123014 - 9 Dec 2025

Cited by 3 | Viewed by 2263

Abstract

The mitochondrial permeability transition pore (mPTP) plays a central role in myocardial injury. Upon reperfusion after myocardial infarction, oxidative stress, calcium overload, and ATP depletion promote mPTP opening, leading to mitochondrial dysfunction, cell death, and infarct expansion. This process affects various cardiac cell [...] Read more.

The mitochondrial permeability transition pore (mPTP) plays a central role in myocardial injury. Upon reperfusion after myocardial infarction, oxidative stress, calcium overload, and ATP depletion promote mPTP opening, leading to mitochondrial dysfunction, cell death, and infarct expansion. This process affects various cardiac cell types differently, contributing to complex pathological remodelling. Key mitochondrial events, such as disruption of bioenergetics parameters, impaired mitophagy, and oxidative stress, drive regulated cell death. Emerging therapies targeting mitochondrial biology, dynamics, and transplantation offer promising strategies to mitigate damage and improve cardiac outcomes. Considering the potential to improve cardiac outcomes and redefine therapeutic approaches in the management of cardiovascular disease, mPTP modulation represents a compelling therapeutic target in myocardial infarction and ischemia–reperfusion injury management. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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15 pages, 3361 KB  

Open AccessArticle

Nuclear Lactate Dehydrogenase A Resists Cardiomyocyte Cell Cycle Arrest Induced by Oxidative Stress

by Mengfei Cao, Jie Luo, Kewei Fu, Yao Xu, Yinyu Wang, Junying Duan, Rui Chen and Wei Yuan

J. Cardiovasc. Dev. Dis. 2025, 12(7), 278; https://doi.org/10.3390/jcdd12070278 - 21 Jul 2025

Cited by 1 | Viewed by 1335

Abstract

A sudden increase in ambient oxygen concentration after birth forces the metabolic switch from anaerobic glycolysis to oxidative phosphorylation, which contributes to the rapid decline of cardiomyocyte proliferation. Lactate dehydrogenase A (LDHA), a metabolic enzyme normally localized in the cytoplasm, has been reported [...] Read more.

A sudden increase in ambient oxygen concentration after birth forces the metabolic switch from anaerobic glycolysis to oxidative phosphorylation, which contributes to the rapid decline of cardiomyocyte proliferation. Lactate dehydrogenase A (LDHA), a metabolic enzyme normally localized in the cytoplasm, has been reported to regulate cardiomyocyte proliferation via inducing metabolic reprogramming. Nuclear LDHA has been observed in multiple proliferative cells, whereas the role of LDHA nuclear translocation in cardiomyocyte proliferation remains unresolved. Here we found that the expression of nuclear LDHA was induced both in the infarct area of myocardial infarction (MI) in mice and hypoxic cardiomyocytes in vitro. Mechanically, mild hypoxia prompted metabolic reprogramming which motivated cardiomyocyte proliferation by alleviating reactive oxygen species (ROS), while severe hypoxia coincided with oxidative stress that induced cardiomyocyte cell cycle arrest. Interestingly, LDHA nuclear translocation in cardiomyocytes occurred in response to oxidative stress, and blocking of nuclear LDHA resulted in elevated ROS generation. Collectively, our findings uncover a non-canonical role of nuclear LDHA in maintaining redox balance and resisting cardiomyocyte cell cycle arrest. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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20 pages, 2891 KB  

Open AccessReview

MAPK, PI3K/Akt Pathways, and GSK-3β Activity in Severe Acute Heart Failure in Intensive Care Patients: An Updated Review

by Massimo Meco, Enrico Giustiniano, Fulvio Nisi, Pierluigi Zulli and Emiliano Agosteo

J. Cardiovasc. Dev. Dis. 2025, 12(7), 266; https://doi.org/10.3390/jcdd12070266 - 10 Jul 2025

Cited by 6 | Viewed by 4478

Abstract

Acute heart failure (AHF) is a clinical syndrome characterized by the sudden onset or rapid worsening of heart failure signs and symptoms, frequently triggered by myocardial ischemia, pressure overload, or cardiotoxic injury. A central component of its pathophysiology is the activation of intracellular [...] Read more.

Acute heart failure (AHF) is a clinical syndrome characterized by the sudden onset or rapid worsening of heart failure signs and symptoms, frequently triggered by myocardial ischemia, pressure overload, or cardiotoxic injury. A central component of its pathophysiology is the activation of intracellular signal transduction cascades that translate extracellular stress into cellular responses. Among these, the mitogen-activated protein kinase (MAPK) pathways have received considerable attention due to their roles in mediating inflammation, apoptosis, hypertrophy, and adverse cardiac remodeling. The canonical MAPK cascades—including extracellular signal-regulated kinases (ERK1/2), p38 MAPK, and c-Jun N-terminal kinases (JNK)—are activated by upstream stimuli such as angiotensin II (Ang II), aldosterone, endothelin-1 (ET-1), and sustained catecholamine release. Additionally, emerging evidence highlights the role of receptor-mediated signaling, cellular stress, and myeloid cell-driven coagulation events in linking MAPK activation to fibrotic remodeling following myocardial infarction. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling cascade plays a central role in regulating cardiomyocyte survival, hypertrophy, energy metabolism, and inflammation. Activation of the PI3K/Akt pathway has been shown to confer cardioprotective effects by enhancing anti-apoptotic and pro-survival signaling; however, aberrant or sustained activation may contribute to maladaptive remodeling and progressive cardiac dysfunction. In the context of AHF, understanding the dual role of this pathway is crucial, as it functions both as a marker of compensatory adaptation and as a potential therapeutic target. Recent reviews and preclinical studies have linked PI3K/Akt activation with reduced myocardial apoptosis and attenuation of pro-inflammatory cascades that exacerbate heart failure. Among the multiple signaling pathways involved, glycogen synthase kinase-3β (GSK-3β) has emerged as a key regulator of apoptosis, inflammation, metabolic homeostasis, and cardiac remodeling. Recent studies underscore its dual function as both a negative regulator of pathological hypertrophy and a modulator of cell survival, making it a compelling therapeutic candidate in acute cardiac settings. While earlier investigations focused primarily on chronic heart failure and long-term remodeling, growing evidence now supports a critical role for GSK-3β dysregulation in acute myocardial stress and injury. This comprehensive review discusses recent advances in our understanding of the MAPK signaling pathway, the PI3K/Akt cascade, and GSK-3β activity in AHF, with a particular emphasis on mechanistic insights, preclinical models, and emerging therapeutic targets. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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20 pages, 2409 KB  

Open AccessReview

The Mechanical Role of YAP/TAZ in the Development of Diabetic Cardiomyopathy

by Jun-Xian Shen, Ling Zhang, Huan-Huan Liu, Zhen-Ye Zhang, Ning Zhao, Jia-Bin Zhou, Ling-Ling Qian and Ru-Xing Wang

Curr. Issues Mol. Biol. 2025, 47(5), 297; https://doi.org/10.3390/cimb47050297 - 23 Apr 2025

Cited by 3 | Viewed by 3149

Abstract

Diabetic cardiomyopathy (DCM) begins with a subclinical stage featuring cardiac hypertrophy, fibrosis, and disrupted signaling. These changes, especially fibrosis and stiffness, often lead to clinical heart failure. The mechanism involves metabolic dysregulation, oxidative stress, and inflammation, leading to cardiac damage and dysfunction. During [...] Read more.

Diabetic cardiomyopathy (DCM) begins with a subclinical stage featuring cardiac hypertrophy, fibrosis, and disrupted signaling. These changes, especially fibrosis and stiffness, often lead to clinical heart failure. The mechanism involves metabolic dysregulation, oxidative stress, and inflammation, leading to cardiac damage and dysfunction. During the progression of the disease, the myocardium senses surrounding mechanical cues, including extracellular matrix properties, tensile tension, shear stress, and pressure load, which significantly influence the pathological remodeling of the heart through mechanotransduction. At the molecular level, the mechanisms by which mechanical cues are sensed and transduced to mediate myocardial mechanical remodeling in DCM remain unclear. The mechanosensitive transcription factors YAP and TAZ fill this gap. This article reviews the latest findings of how YAP and TAZ perceive a wide range of mechanical cues, from shear stress to extracellular matrix stiffness. We focus on how these cues are relayed through the cytoskeleton to the nucleus, where they trigger downstream gene expression. Here, we review recent progress on the crucial role of YAP and TAZ mechanotransduction in the pathological changes observed in DCM, including myocardial fibrosis, hypertrophy, inflammation, mitochondrial dysfunction, and cell death. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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29 pages, 1249 KB  

Open AccessReview

The Application and Molecular Mechanisms of Mitochondria-Targeted Antioxidants in Chemotherapy-Induced Cardiac Injury

by Chih-Jen Liu, Lu-Kai Wang and Fu-Ming Tsai

Curr. Issues Mol. Biol. 2025, 47(3), 176; https://doi.org/10.3390/cimb47030176 - 7 Mar 2025

Cited by 19 | Viewed by 4803

Abstract

Chemotherapeutic agents play a crucial role in cancer treatment. However, their use is often associated with significant adverse effects, particularly cardiotoxicity. Drugs such as anthracyclines (e.g., doxorubicin) and platinum-based agents (e.g., cisplatin) cause mitochondrial damage, which is one of the main mechanisms underlying [...] Read more.

Chemotherapeutic agents play a crucial role in cancer treatment. However, their use is often associated with significant adverse effects, particularly cardiotoxicity. Drugs such as anthracyclines (e.g., doxorubicin) and platinum-based agents (e.g., cisplatin) cause mitochondrial damage, which is one of the main mechanisms underlying cardiotoxicity. These drugs induce oxidative stress, leading to an increase in reactive oxygen species (ROS), which in turn damage the mitochondria in cardiomyocytes, resulting in impaired cardiac function and heart failure. Mitochondria-targeted antioxidants (MTAs) have emerged as a promising cardioprotective strategy, offering a potential solution. These agents efficiently scavenge ROS within the mitochondria, protecting cardiomyocytes from oxidative damage. Recent studies have shown that MTAs, such as elamipretide, SkQ1, CoQ10, and melatonin, significantly mitigate chemotherapy-induced cardiotoxicity. These antioxidants not only reduce oxidative damage but also help maintain mitochondrial structure and function, stabilize mitochondrial membrane potential, and prevent excessive opening of the mitochondrial permeability transition pore, thus preventing apoptosis and cardiac dysfunction. In this review, we integrate recent findings to elucidate the mechanisms of chemotherapy-induced cardiotoxicity and highlight the substantial therapeutic potential of MTAs in reducing chemotherapy-induced heart damage. These agents are expected to offer safer and more effective treatment options for cancer patients in clinical practice. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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23 pages, 7444 KB  

Open AccessArticle

Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment

by Yuya Yoshida, Naoki Nishikawa, Kohei Fukuoka, Akito Tsuruta, Kaita Otsuki, Taiki Fukuda, Yuma Terada, Tomohito Tanihara, Taisei Kumamoto, Ryotaro Tsukamoto, Takumi Nishi, Kosuke Oyama, Kengo Hamamura, Kouta Mayanagi, Satoru Koyanagi, Shigehiro Ohdo and Naoya Matsunaga

Int. J. Mol. Sci. 2024, 25(23), 13009; https://doi.org/10.3390/ijms252313009 - 3 Dec 2024

Cited by 3 | Viewed by 3068

Abstract

Defects in Aryl hydrocarbon receptor nuclear translocator-like 1 (ARNTL), a central component of the circadian clock mechanism, may promote or inhibit the induction of inflammation by monocytes/macrophages, with varying effects on different diseases. However, ARNTL’s role in monocytes/macrophages under chronic kidney disease (CKD), [...] Read more.

Defects in Aryl hydrocarbon receptor nuclear translocator-like 1 (ARNTL), a central component of the circadian clock mechanism, may promote or inhibit the induction of inflammation by monocytes/macrophages, with varying effects on different diseases. However, ARNTL’s role in monocytes/macrophages under chronic kidney disease (CKD), which presents with systemic inflammation, is unclear. Here, we report that the expression of Arntl in monocytes promoted CKD-induced cardiac damage. The expression of G-protein-coupled receptor 68 (GPR68), which exacerbates CKD-induced cardiac disease, was regulated by ARNTL. Under CKD conditions, GPR68 expression was elevated via ARNTL, particularly in the presence of PU.1, a transcription factor specific to monocytes and macrophages. In CKD mouse models lacking monocyte-specific ARNTL, GPR68 expression in monocytes was reduced, leading to decreased cardiac damage and fibrosis despite no improvement in renal excretory capacity or renal fibrosis and increased angiotensin II production. The loss of ARNTL did not affect the expression of marker molecules, indicating the origin or differentiation of cardiac macrophages, but affected GPR68 expression only in cardiac macrophages derived from mature monocytes, highlighting the significance of the interplay between GPR68 and ARNTL in monocytes/macrophages and its influence on cardiac pathology. Understanding this complex relationship between circadian clock mechanisms and disease could help uncover novel therapeutic strategies. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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12 pages, 694 KB  

Open AccessArticle

A Multi-Biomarker Approach to Increase the Accuracy of Diagnosis and Management of Coronary Artery Disease

by Lenka Hostačná, Jana Mašlanková, Dominik Pella, Beáta Hubková, Mária Mareková and Daniel Pella

J. Cardiovasc. Dev. Dis. 2024, 11(9), 258; https://doi.org/10.3390/jcdd11090258 - 23 Aug 2024

Cited by 5 | Viewed by 2542

Abstract

Non-invasive possibilities of predicting cardiovascular risk and monitoring the treatment and progression of coronary artery disease (CAD) are important subjects of cardiovascular research. Various inflammatory markers have been identified as potential biomarkers of CAD, including interleukin-6 (IL-6), lipocalin-2 (LCN-2), growth differentiation factor 15 [...] Read more.

Non-invasive possibilities of predicting cardiovascular risk and monitoring the treatment and progression of coronary artery disease (CAD) are important subjects of cardiovascular research. Various inflammatory markers have been identified as potential biomarkers of CAD, including interleukin-6 (IL-6), lipocalin-2 (LCN-2), growth differentiation factor 15 (GDF-15), and T cell immunoglobulin and mucin domain-3 (TIM-3). This research aims to identify their utility in the investigation of CAD severity and progression. The basic anthropometric parameters, as well as the levels of urea, creatinine, CRP, leukocytes, fibrinogen, and biomarkers of inflammation, were measured in 130 patients who underwent coronary angiography. In male patients, divided according to findings on coronary angiography, we observed an increasing expression of GDF-15 with increasing stenosis (with worsening findings). In females, we observed increasing fibrinogen expression with increasing stenosis, i.e., findings on coronary angiography. Correlation analysis did not confirm the relationship between TIM-3, LCN and 2, IL-6 and the severity of findings obtained by coronary angiography; however, the correlation of TIM-3 and LCN-2 expression was positive with the finding, and the correlation of IL-6 with the finding was surprisingly negative. Understanding the role of these inflammatory markers in CAD can be helpful in risk stratification, guiding therapeutic strategies, and monitoring treatment responses in patients with CAD. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)

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