Exploring bradykinin: A common mediator in the pathophysiology of sepsis and atherosclerotic cardiovascular disease.
Vascul Pharmacol
; 156: 107414, 2024 Sep.
Article
en En
| MEDLINE
| ID: mdl-39089528
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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Sistema Renina-Angiotensina
/
Coagulación Sanguínea
/
Bradiquinina
/
Transducción de Señal
/
Sepsis
/
Aterosclerosis
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Vascul Pharmacol
Asunto de la revista:
ANGIOLOGIA
/
FARMACOLOGIA
Año:
2024
Tipo del documento:
Article
Pais de publicación:
Estados Unidos