Dysregulated redox signalling, mitochondrial dysfunction and impaired autophagy are interconnected mechanisms that orchestrate inflammatory and immune responses during cardiovascular disease progression. Inflammation is largely modulated by altered redox signalling, which primarily involves reactive oxygen and nitrogen species (ROS/RNS). Mitochondria are essential for energy production and cellular homeostasis, but their dysfunction leads to the accumulation of excessive ROS, which triggers inflammation. This pro-oxidative milieu disrupts immune regulation by activating inflammasomes, promoting cytokine secretion, triggering immune cell infiltration and ultimately contributing to cardiovascular injury. Conversely, intracellular degradation processes such as mitophagy, alleviates these effects by selectively eliminating dysfunctional mitochondria, thereby decreasing ROS levels and maintaining immune homoeostasis. These interconnected processes influence myeloid cell function including macrophage polarization, dendritic cell activation, and neutrophil activity. The modulation of these immune responses is crucial for determining the severity and resolution of cardiac and vascular inflammation, and consequently the extent of cellular injury. This review examines the latest developments and understanding of the intricate relationships between redox signalling, mitochondrial dysfunction, autophagy and oxidative stress in modulating inflammation and immune responses in cardiovascular diseases. Understanding these interrelationships will inform future studies and therapeutic solutions for the prevention and treatment of cardiovascular diseases.
Pervin et al. (2025) studied this question.