Exploring bradykinin: A common mediator in the pathophysiology of sepsis and atherosclerotic cardiovascular disease
Document Type
Article
Publication Date
9-1-2024
Abstract
Sepsis and atherosclerotic cardiovascular disease (ASCVD) are major health challenges involving complex processes like inflammation, renin-angiotensin system (RAS) dysregulation, and thrombosis. Despite distinct clinical symptoms, both conditions share mechanisms mediated by bradykinin. This review explores bradykinin's role in inflammation, RAS modulation, and thrombosis in sepsis and ASCVD. In sepsis, variable kininogen-bradykinin levels may correlate with disease severity and progression, though the effect of bradykinin receptor modulation on inflammation remains uncertain. RAS activation is present in both diseases, with sepsis showing variable or low levels of Ang II, ACE, and ACE2, while ASCVD consistently exhibits elevated levels. Bradykinin may act as a mediator for ACE2 and AT2 receptor effects in RAS regulation. It may influence clotting and fibrinolysis in sepsis-associated coagulopathy, but evidence for an antithrombotic effect in ASCVD is insufficient. Understanding bradykinin's role in these shared pathologies could guide therapeutic and monitoring strategies and inform future research.
Keywords
Bradykinin, Sepsis, Atherosclerosis, Inflammation, Angiotensin
Divisions
phartech
Funders
Universiti Sultan Zainal Abidin (UniSZA/2021/DPU1.0/15 (R0319))
Publication Title
Vascular Pharmacology
Volume
156
Publisher
Elsevier
Publisher Location
STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA