Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.
Zhigang LiYilei MengChang LiuHuan LiuWenze CaoChang TongMin LuLi LiLuying PengPublished in: Cell proliferation (2020)
Kcnh2 plays a protection role in sepsis-induced cardiac dysfunction (SCID) via regulating FAK/AKT-FOXO3A to block LPS-induced myocardium apoptosis, indicating a potential effect of the potassium channels in pathophysiology of SCID.
Keyphrases
- lps induced
- signaling pathway
- oxidative stress
- diabetic rats
- high glucose
- intensive care unit
- acute kidney injury
- inflammatory response
- cell proliferation
- transcription factor
- left ventricular
- pi k akt
- septic shock
- drug induced
- endoplasmic reticulum stress
- cell death
- cell cycle arrest
- cell migration
- heart failure
- atrial fibrillation
- stress induced