Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.

ABSTRACT:

Objectives

Myocardial dysfunction is a significant manifestation in sepsis, which results in high mortality. Even Kcnh2 has been hinted to associate with the pathological process, its involved signalling is still elusive.

Materials and methods

The caecal ligation puncture (CLP) surgery or lipopolysaccharide (LPS) injection was performed to induce septic cardiac dysfunction. Western blotting was used to determine KCNH2 expression. Cardiac function was examined by echocardiography 6 hours after CLP and LPS injection in Kcnh2 knockout (Kcnh2^+/- ) and NS1643 injection rats (n ≥ 6/group). Survival was monitored following CLP-induced sepsis (n ≥ 8/group).

Results

Sepsis could downregulate KCNH2 level in the rat heart, as well as in LPS-stimulated cardiomyocytes b

SUBMITTER: Li Z 

PROVIDER: S-EPMC7848965 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature