Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell DOI Creative Commons
Ioannis Paraskevaidis, Christos Kourek, Dimitrios Farmakis

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(12), P. 1534 - 1534

Published: Nov. 29, 2024

Myocardial cells and the extracellular matrix achieve their functions through availability of energy. In fact, mechanical electrical properties heart are heavily dependent on balance between energy production consumption. The produced is utilized in various forms, including kinetic, dynamic, thermal Although total remains nearly constant, contribution each form changes over time. Thermal increases, while dynamic kinetic decrease, ultimately becoming insufficient to adequately support cardiac function. As a result, toxic byproducts, unfolded or misfolded proteins, free radicals, other harmful substances accumulate within myocardium. This leads failure crucial processes such as myocardial contraction–relaxation coupling, ion exchange, cell growth, regulation apoptosis necrosis. Consequently, both micro- macro-architecture altered. Energy consumption depend heart’s metabolic resources functional state structure, cardiomyocytes, non-cardiomyocyte cells, energetic behavior. Mitochondria, which intracellular organelles that produce more than 95% ATP, play critical role fulfilling all these requirements. Therefore, it essential gain deeper understanding anatomy, function, homeostatic properties.

Language: Английский

Mitochondrial Dysfunction in Cardiovascular Diseases DOI Open Access
Han‐Mo Yang

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 1917 - 1917

Published: Feb. 23, 2025

Mitochondrial dysfunction is increasingly recognized as a central contributor to the pathogenesis of cardiovascular diseases (CVDs), including heart failure, ischemic disease, hypertension, and cardiomyopathy. Mitochondria, known powerhouses cell, play vital role in maintaining cardiac energy homeostasis, regulating reactive oxygen species (ROS) production controlling cell death pathways. Dysregulated mitochondrial function results impaired adenosine triphosphate (ATP) production, excessive ROS generation, activation apoptotic necrotic pathways, collectively driving progression CVDs. This review provides detailed examination molecular mechanisms underlying CVDs, mutations DNA (mtDNA), defects oxidative phosphorylation (OXPHOS), alterations dynamics (fusion, fission, mitophagy). Additionally, specific conditions explored, highlighting its impact on endothelial dysfunction, myocardial remodeling, arrhythmias. Emerging therapeutic strategies targeting such antioxidants, metabolic modulators, gene therapy, are also discussed. By synthesizing recent advances biology research, this aims enhance understanding mitochondria CVDs identify potential targets improve outcomes.

Language: Английский

Citations

0
MAP Kinase Phosphatase-5 Deficiency Improves Endurance Exercise Capacity DOI Creative Commons
Jaime A. Perales, Ahmed Lawan, Sudip Bajpeyi

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(6), P. 410 - 410

Published: March 11, 2025

Aerobic exercise promotes physiological cardiac adaptations, improving cardiovascular function and endurance capacity. However, the molecular mechanisms by which aerobic induces adaptations enhances performance remain poorly understood. Mitogen-activated protein kinase (MAPK) phosphatase-5 (MKP-5) is highly expressed in muscle, indicating its potential role function. This study investigates of MKP-5 early response to muscle using MKP-5-deficient (Mkp-5-/-) wild-type (Mkp-5+/+) mice. Mice were subjected a 5-day treadmill training program after habituation. After exercise, progressive stress test was performed evaluate Our results revealed that exercised mice exhibited significant reduction gene expression compared sedentary (0.19 ± 5.89-fold; p < 0.0001). Mkp-5-/- achieved significantly greater endurance, with running distance (2.81 169.8-fold; 0.0429) longer than Mkp-5+/+ Additionally, deficiency enhanced Akt/mTOR signaling (p-Akt/Akt: 1.29 0.12-fold; = 0.04; p-mTOR/mTOR: 1.59 0.14-fold; 0.002) mitochondrial biogenesis (pgc-1α: 1.56 0.27-fold; 0.03) exercise. Furthermore, markers cardiomyocyte proliferation, including PCNA (2.24 0.31-fold; 0.001), GATA4 (1.47 0.10-fold; CITED4 (2.03 0.15-fold; 0.0001) upregulated hearts following These findings demonstrated plays critical regulating key pathways for exercise-induced highlighting contribution enhancing health

Language: Английский

Citations

0
Aconiti Lateralis Radix Praeparata ameliorates heart failure via PI3K/AKT/Bnip3 pathway DOI Creative Commons
Wenxiu Liu,

Xingju Zou,

Yang Zheng

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 26, 2025

Background Chronic heart failure (CHF) is one of the leading causes high mortality worldwide. It characterized by pathological hypertrophy and poses a major threat to human health. Aconiti Lateralis Radix Praeparata widely used in ancient China treat CHF. However, pathology obscured, necessitating further exploration. Methods Prospective targets were predicted network analysis. A transverse aortic constriction (TAC) mice model was subsequently constructed determine effects aqueous extract (AEA) on The echocardiography performed investigate cardiac function. Histopathological analysis tissue conducted assess myocardial fibrosis. Nontargeted metabolomics analyze serum metabolites. phosphorylation level PI3K AKT, downstream such as Bnip3, p62, Atg5, LC3II measured Western blotting. In vitro , norepinephrine (NE) stimulate hypertrophy. Parameters reactive oxygen species levels, mitochondrial membrane potential, ATP concentration, CK/MB content detected H9c2 cells. Results AEA significantly alleviated Network indicated participation AKT CHF, modulated Praeparata. vivo administration effectively ameliorated performance, evidenced elevation ejection fraction. displayed diminishment collagen fiber. Metabolomics showed that several metabolites tetrahydroxycorticosterone, decylubiquinone taurocholic acid increased TAC serum. Additionally, levels expression Drp1, Opa1, Atg5 altered group. NE stimulation cell surface area deteriorated functions partially reversed results, mechanism associated with mitophagy. Conclusion This study revealed improved function via PI3K/AKT/Bnip3 pathway.

Language: Английский

Citations

0
Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell DOI Creative Commons
Ioannis Paraskevaidis, Christos Kourek, Dimitrios Farmakis

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(12), P. 1534 - 1534

Published: Nov. 29, 2024

Myocardial cells and the extracellular matrix achieve their functions through availability of energy. In fact, mechanical electrical properties heart are heavily dependent on balance between energy production consumption. The produced is utilized in various forms, including kinetic, dynamic, thermal Although total remains nearly constant, contribution each form changes over time. Thermal increases, while dynamic kinetic decrease, ultimately becoming insufficient to adequately support cardiac function. As a result, toxic byproducts, unfolded or misfolded proteins, free radicals, other harmful substances accumulate within myocardium. This leads failure crucial processes such as myocardial contraction–relaxation coupling, ion exchange, cell growth, regulation apoptosis necrosis. Consequently, both micro- macro-architecture altered. Energy consumption depend heart’s metabolic resources functional state structure, cardiomyocytes, non-cardiomyocyte cells, energetic behavior. Mitochondria, which intracellular organelles that produce more than 95% ATP, play critical role fulfilling all these requirements. Therefore, it essential gain deeper understanding anatomy, function, homeostatic properties.

Language: Английский

Citations

2