Reimagining risk stratification: Dipeptidyl peptidase 3 in the new era of cardiovascular biomarkers

Figure 1 Schematic representation of dipeptidyl peptidase 3 release during cellular stress and its downstream effects. Cellular stress (e.g., ischemia, acute coronary syndrome, shock) triggers the release of intracellular dipeptidyl peptidase 3 (DPP3) into the plasma. Extracellular DPP3 degrades angiotensin II, leading to impaired renin-angiotensin-aldosterone system signaling. This cascade results in hemodynamic effects such as vasodilation, hypotension, and negative inotropy, as well as systemic consequences including inflammation, organ hypoperfusion, and progression toward a shock spiral. Potential therapeutic interventions include anti-cDPP3 antibodies and supportive therapies aimed at restoring hemodynamic stability and mitigating systemic damage. DPP3: Dipeptidyl peptidase 3.