Model Systems for Addressing Mechanism of Arrhythmogenesis in Cardiac Repair

Abstract

Purpose of Review Cardiac cell-based therapy represents a promising approach for cardiac repair. However, one of the main challenges is cardiac arrhythmias associated with stem cell transplantation. The current review summarizes the recent progress in model systems for addressing mechanisms of arrhythmogenesis in cardiac repair. Recent Findings Animal models have been extensively developed for mechanistic studies of cardiac arrhythmogenesis. Advances in human induced pluripotent stem cells (hiPSCs), patient-specific disease models, tissue engineering, and gene editing have greatly enhanced our ability to probe the mechanistic bases of cardiac arrhythmias. Additionally, recent development in multiscale computational studies and machine learning provides yet another powerful tool to quantitatively decipher the mechanisms of cardiac arrhythmias. Summary Advancing efforts towards the integrations of experimental and computational studies are critical to gain insights into novel mitigation strategies for cardiac arrhythmias in cell-based therapy.

Inflammation and arrhythmogenesis: a narrative review of the complex relationship

“…A vital component of cardiac muscle cell contraction is calcium. Increased Table 1 Indicators of systemic inflammation and incident arrhythmia risk-observational study summary UKB UK Biobank, HR hazard ratio, VA ventricular arrhythmia, AF atrial fibrillation/flutter, CRP C-reactive protein, NLR neutrophil-to-lymphocyte ratio, SII systemic immune-inflammation index, PLR platelet-to-lymphocyte ratio, LMR lymphocyte-to-monocyte ratio sarcoplasmic reticulum (SR) calcium leak and reduced SR calcium absorption brought on by inflammatory cytokines can both lead to cytosolic calcium excess [26]. This capacity to induce spontaneous calcium waves and delayed after-depolarizations (DADs) may lead to arrhythmias [27].…”