Neuroinflammation in heart failure: new insights for an old disease

Diaz, Hugo S.; Toledo, Camilo; Andrade, David C.; Marcus, Noah J.; del Rio, Rodrigo

Abstract

Heart failure (HF) is a complex clinical syndrome affecting roughly 26 million people worldwide. Increased sympathetic drive is a hallmark of HF and is associated with disease progression and higher mortality risk. Several mechanisms contribute to enhanced sympathetic activity in HF, but these pathways are still incompletely understood. Previous work suggests that inflammation and activation of the renin-angiotensin system (RAS) increases sympathetic drive. Importantly, chronic inflammation in several brain regions is commonly observed in aged populations, and a growing body of evidence suggests neuroinflammation plays a crucial role in HF. In animal models of HF, central inhibition of RAS and pro-inflammatory cytokines normalizes sympathetic drive and improves cardiac function. The precise molecular and cellular mechanisms that lead to neuroinflammation and its effect on HF progression remain undetermined. This review summarizes the most recent advances in the field of neuroinflammation and autonomic control in HF. In addition, it focuses on cellular and molecular mediators of neuroinflammation in HF and in particular on brain regions involved in sympathetic control. Finally, we will comment on what is known about neuroinflammation in the context of preserved vs. reduced ejection fraction HF.

Más información

Título según WOS: Neuroinflammation in heart failure: new insights for an old disease
Título según SCOPUS: Neuroinflammation in heart failure: new insights for an old disease
Título de la Revista: JOURNAL OF PHYSIOLOGY-LONDON
Volumen: 598
Número: 1
Editorial: Wiley
Fecha de publicación: 2020
Página de inicio: 33
Página final: 59
Idioma: English
DOI:

10.1113/JP278864

Notas: ISI, SCOPUS