Crosstalk between the renin-angiotensin system and the endoplasmic reticulum stress in the cardiovascular system:...

Area of Science:

• Cardiovascular Science
• Endocrinology
• Molecular Biology

Background:

• The renin-angiotensin system (RAS) plays a crucial role in cardiovascular homeostasis.
• Overactivation of the classical RAS arm (ACE/Ang-II/AT1R) is linked to cardiovascular diseases and endoplasmic reticulum (ER) stress.
• ER stress can lead to heart failure, atherosclerosis, hypertension, and endothelial dysfunction.

Purpose of the Study:

• To explore the role of the classical RAS arm in activating the unfolded protein response (UPR).
• To investigate the potential protective role of the counter-regulatory RAS arm (ACE-2/Ang-(1-7)/Mas receptor) in mitigating ER stress.
• To clarify the crosstalk mechanisms between RAS arms and ER stress.

Main Methods:

• Review of existing in vivo and in vitro studies.
• Analysis of evidence linking Ang-II treatment to increased ER stress markers.
• Examination of studies on RAS blockers, gene silencing, and genetic models affecting ER stress.

Main Results:

• Ang-II treatment increases ER stress markers.
• Targeting the classical RAS arm reduces ER stress markers.
• Limited evidence suggests protective effects of the counter-regulatory RAS arm against ER stress.

Conclusions:

• The classical RAS arm is a key mechanism in UPR activation.
• The counter-regulatory RAS arm may offer protection against ER stress.
• Further research is needed to elucidate the crosstalk mechanisms between RAS arms and ER stress.