REVIEW article
Front. Cardiovasc. Med.
Sec. Hypertension
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1623775
This article is part of the Research TopicEmerging Molecules in Pulmonary Hypertension: Diagnosis, Risk Prediction, Treatment and PrognosisView all 5 articles
Exploring the Interplay between Mitochondria and Endoplasmic Reticulum in Pulmonary Arterial Hypertension
Provisionally accepted- Depatment of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Pulmonary arterial hypertension (PAH) is a subtype of pulmonary hypertension (PH), characterized by pulmonary arterial remodeling. This disease frequently progresses to right heart failure and can result in patient mortality. Research at the cellular and molecular level is gradually revealing the mechanism underlying the development of pulmonary arterial hypertension, providing new avenues for treatment by identifying potential therapeutic targets. Contact between the endoplasmic reticulum and mitochondria has been recognized for several decades. And an increasing number of laboratory and clinical studies are beginning to elucidate the relationship between PAH and the interplay involving mitochondria and the endoplasmic reticulum. In this review, we first introduce the basic normal biological functions and processes of MAM-based mitochondrial-endoplasmic reticulum interactions. We then discuss how the dysfunction contributes to pulmonary arterial hypertension (PAH), focusing on three key aspects: mitochondrial dynamics, calcium homeostasis, and endoplasmic reticulum stress. Clarifying these issues may provide important insights for therapeutic interventions in PAH.
Keywords: pulmonary arterial hypertension, mitochondria-associated endoplasmic reticulum membranes, mitochondrial dynamics, Calcium, er stress
Received: 06 May 2025; Accepted: 16 Oct 2025.
Copyright: © 2025 He and Liao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuanzhou He, yuanzhouhe84@163.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.