Abstract
Background and Aims: chronic induction of endoplasmic reticulum (ER) stress and its deleterious relationship with mitochondria are responsible for triggering pathological mechanisms involved in the physiopathology of cardiovascular disease. Therefore, we aim to determine whether inhibition of ER stress is effective to reduce abdominal aortic aneurysm (AAA) development and hypertensive cardiac hypertrophy in an experimental model.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
