Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights
AbstractCardiovascular diseases and cancer are the leading causes of death in the Western world and share common risk factors. Reduced cardiorespiratory fitness (CRF) is a major determinant of cardiovascular morbidity and cancer survival. In this review we discuss cancer- induced disturbances of parenchymal, cellular, and mitochondrial function, which limit CRF and may be antagonized and attenuated through exercise training. We show the impact of CRF on cancer survival and its attenuating effects on cardiotoxicity of cancer-related treatment. Tailored exercise programs are not yet available for each tumor entity as several...
Source: Basic Research in Cardiology - February 14, 2024 Category: Cardiology Source Type: research
Distinct cytoskeletal regulators of mechanical memory in cardiac fibroblasts and cardiomyocytes
AbstractRecognizing that cells “feel” and respond to their mechanical environment, recent studies demonstrate that many cells exhibit a phenomenon of “mechanical memory” in which features induced by prior mechanical cues persist after the mechanical stimulus has ceased. While there is a general recognition that different cell types exhibit different responses to changes in extracellular matrix stiffening, the phenomenon of mechanical memory within myocardial cell types has received little attention to date. To probe the dynamics of mechanical memory in cardiac fibroblasts (CFs) and cardiomyocytes derived from human...
Source: Basic Research in Cardiology - February 13, 2024 Category: Cardiology Source Type: research
Mineralocorticoid receptor promotes cardiac macrophage inflammaging
This study highlights the MR as an important mediator of cardiac macrophage inflammaging and age-related fibrotic remodeling. (Source: Basic Research in Cardiology)
Source: Basic Research in Cardiology - February 8, 2024 Category: Cardiology Source Type: research
The interplay of collagen, macrophages, and microcalcification in atherosclerotic plaque cap rupture mechanics
AbstractThe rupture of an atherosclerotic plaque cap overlying a lipid pool and/or necrotic core can lead to thrombotic cardiovascular events. In essence, the rupture of the plaque cap is a mechanical event, which occurs when the local stress exceeds the local tissue strength. However, due to inter- and intra-cap heterogeneity, the resulting ultimate cap strength varies, causing proper assessment of the plaque at risk of rupture to be lacking. Important players involved in tissue strength include the load-bearing collagenous matrix, macrophages, as major promoters of extracellular matrix degradation, and microcalcification...
Source: Basic Research in Cardiology - February 8, 2024 Category: Cardiology Source Type: research
Mineralocorticoid receptor promotes cardiac macrophage inflammaging
This study highlights the MR as an important mediator of cardiac macrophage inflammaging and age-related fibrotic remodeling. (Source: Basic Research in Cardiology)
Source: Basic Research in Cardiology - February 8, 2024 Category: Cardiology Source Type: research
The interplay of collagen, macrophages, and microcalcification in atherosclerotic plaque cap rupture mechanics
AbstractThe rupture of an atherosclerotic plaque cap overlying a lipid pool and/or necrotic core can lead to thrombotic cardiovascular events. In essence, the rupture of the plaque cap is a mechanical event, which occurs when the local stress exceeds the local tissue strength. However, due to inter- and intra-cap heterogeneity, the resulting ultimate cap strength varies, causing proper assessment of the plaque at risk of rupture to be lacking. Important players involved in tissue strength include the load-bearing collagenous matrix, macrophages, as major promoters of extracellular matrix degradation, and microcalcification...
Source: Basic Research in Cardiology - February 8, 2024 Category: Cardiology Source Type: research
Statins affect human iPSC-derived cardiomyocytes by interfering with mitochondrial function and intracellular acidification
AbstractStatins are effective drugs in reducing cardiovascular morbidity and mortality by inhibiting cholesterol synthesis. These effects are primarily beneficial for the patient ’s vascular system. A significant number of statin users suffer from muscle complaints probably due to mitochondrial dysfunction, a mechanism that has recently been elucidated. This has raised our interest in exploring the effects of statins on cardiac muscle cells in an era where the elderly and patients with poorer functioning hearts and less metabolic spare capacity start dominating our patient population. Here, we investigated the effects of...
Source: Basic Research in Cardiology - February 2, 2024 Category: Cardiology Source Type: research
Acute antiarrhythmic effects of SGLT2 inhibitors –dapagliflozin lowers the excitability of atrial cardiomyocytes
In this study, we place special emphasis on the atria and investigate acute electrophysiological effects of dapagliflozin to assess the antiarrhythmic potential of SGLT2 inhibitors. Direct electrophysiological effects of dapagliflozin were investigated in patch clamp experiments on isolated atrial cardiomyocytes. Acute treatment with elevated-dose dapagliflozin caused a significant reduction of the action potential inducibility, the amplitude and maximum upstroke velocity. The inhibitory effects were reproduced in human induced pluripotent stem cell-derived cardiomyocytes, and were more pronounced in atrial compared to ven...
Source: Basic Research in Cardiology - February 1, 2024 Category: Cardiology Source Type: research
Striated preferentially expressed gene deficiency leads to mitochondrial dysfunction in developing cardiomyocytes
AbstractA deficiency of striated preferentially expressed gene (Speg), a member of the myosin light chain kinase family, results in abnormal myofibril structure and function of immature cardiomyocytes (CMs), corresponding with a dilated cardiomyopathy, heart failure and perinatal death. Mitochondrial development plays a role in cardiomyocyte maturation. Therefore, this study investigated whetherSpeg deficiency ( – / – ) in CMs would result in mitochondrial abnormalities.Speg wild-type andSpeg−/− C57BL/6 littermate mice were utilized for assessment of mitochondrial structure by transmission electron and confocal m...
Source: Basic Research in Cardiology - February 1, 2024 Category: Cardiology Source Type: research
Mast cell stabilizer, an anti-allergic drug, reduces ventricular arrhythmia risk via modulation of neuroimmune interaction
AbstractMast cells (MCs) are important intermediates between the nervous and immune systems. The cardiac autonomic nervous system (CANS) crucially modulates cardiac electrophysiology and arrhythmogenesis, but whether and how MC-CANS neuroimmune interaction influences arrhythmia remain unclear. Our clinical data showed a close relationship between serum levels of MC markers and CANS activity, and then we use mast cell stabilizers (MCSs) to alter this MC-CANS communication. MCSs, which are well-known anti-allergic agents, could reduce the risk of ventricular arrhythmia (VA) after myocardial infarction (MI). RNA-sequencing (R...
Source: Basic Research in Cardiology - February 1, 2024 Category: Cardiology Source Type: research
Targeted ablation of the left middle cervical ganglion prevents ventricular arrhythmias and cardiac injury induced by AMI
In conclusion, this study demonstrated that LMCG ablation suppressed cardiac sympathetic activity, stabilized ventricular electrophysiological properties and mitigated cardiomyocyte death, resultantly preventing ischemia-induced ventricular arrhythmias, myocardial injury, and cardiac dysfunction. Neuromodulation therapy targeting LMCG represented a promising strategy for the treatment of AMI. (Source: Basic Research in Cardiology)
Source: Basic Research in Cardiology - February 1, 2024 Category: Cardiology Source Type: research
Thrombospondin 1 and Reelin act through Vldlr to regulate cardiac growth and repair
AbstractAdult mammalian cardiomyocytes have minimal cell cycle capacity, which leads to poor regeneration after cardiac injury such as myocardial infarction. Many positive regulators of cardiomyocyte cell cycle and cardioprotective signals have been identified, but extracellular signals that suppress cardiomyocyte proliferation are poorly understood. We profiled receptors enriched in postnatal cardiomyocytes, and found that very-low-density-lipoprotein receptor (Vldlr) inhibits neonatal cardiomyocyte cell cycle. Paradoxically, Reelin, the well-known Vldlr ligand, expressed in cardiac Schwann cells and lymphatic endothelial...
Source: Basic Research in Cardiology - February 1, 2024 Category: Cardiology Source Type: research
