Cardioprotective mechanotransduction pathway of the coronary venous microcirculation (PICSO-related signaling)

Activation/modulation of cardioprotective molecular pathways related to pressure variations in the coronary venous microcirculation is a physiological mechanism triggered by mechanical interventions such as Pressure-controlled Intermittent Coronary Sinus Occlusion (PICSO). This process is characterized by the elevation of pressure within the coronary venous system, which creates shear stress on the vascular endothelium and redistributes blood flow to the ischemic border zones (Mohl et al., 2008). The mechanical stimulus activates mechanotransduction pathways that upregulate several cardioprotective factors, including Vascular Endothelial Growth Factor (VEGF), Heme Oxygenase-1 (HO-1), and Nitric Oxide (NO) (Mohl et al., 2011). These molecular responses are intended to salvage myocardium, reduce infarct size, and improve long-term ventricular function in patients undergoing treatment for acute myocardial infarction (De Maria et al., 2018). As this 'target' represents a complex physiological response and a device-based clinical strategy rather than a single molecule, it is not targeted by specific pharmacological agents, though it intersects with endogenous survival signaling pathways (Heusch, 2015). Research suggests that optimizing the timing and pressure of these venous variations can significantly enhance the endogenous regenerative capacity of the heart.

Other names

Pressure-controlled intermittent coronary sinus occlusion signalingCoronary sinus mechanotransductionPICSO-induced cardioprotectionVenous microcirculation pressure-driven pathway

Activation of endothelial mechanoreceptors via periodic elevation of coronary sinus pressure, which induces the expression of cytoprotective genes and growth factors through shear stress-mediated signaling.