Up-regulated Expression of a TOR2A Gene Product-Salusin-β in the Paraventricular Nucleus Enhances Sympathetic Activity and Cardiac Sympathetic Afferent Reflex in Rats with Chronic Heart Failure Induced by Coronary Artery Ligation.
Yu XuXuejie FeiHangjiang FuAidong ChenXinrui ZhuFeng ZhangYing HanPublished in: Acta physiologica (Oxford, England) (2023)
Increased salusin-β activity in the PVN contributes to sympathetic hyperactivation and CSAR in CHF by inhibiting NO release and stimulating NAD(P)H oxidase-ROS production. Reducing endogenous central salusin-β expression might be a novel strategy for preventing and treating CHF in the future.
Keyphrases
- poor prognosis
- coronary artery
- left ventricular
- binding protein
- dna damage
- genome wide
- pulmonary artery
- signaling pathway
- cell death
- long non coding rna
- copy number
- reactive oxygen species
- dna methylation
- oxidative stress
- ejection fraction
- transcription factor
- pulmonary hypertension
- pulmonary arterial hypertension
- genome wide identification