Yang Yang
Yi Luan- Clinical Systems Biology Research Laboratories, Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Editorial on the Research Topic
Recent advances in mitochondria-associated endoplasmic reticulum membranes (MAMs) in heart-related diseases
Mitochondria-associated endoplasmic reticulum membranes (MAMs) are the physical connections between the two important organelles of the endoplasmic reticulum and mitochondria, and also the key to the normal functioning of the endoplasmic reticulum and mitochondria (1). It enables Ca2+ to be efficiently transported from the endoplasmic reticulum to the mitochondria, and is involved in the regulation of ROS, lipid metabolism, cell apoptosis, etc., so as to maintain cell metabolism and normal function (2). The concept of MAMs was proposed by John Ruby et al. as early as 1969 and was not isolated from rat livers until 1990 by Jean Vance (3). In the following 30 years, with the development of electron microscopy, high resolution imaging and other technologies, people have a clear and multi-level understanding of the important functions of MAMs.
By mass spectrometry, more than 1,000 proteins have been found to be concentrated in MAMs structures, and many of these proteins have been found to affect the progression of cardiovascular diseases. Studies have shown that MAMs play an important role in the development of cardiovascular diseases such as heart failure, myocardial ischemia-reperfusion injury, and atherosclerosis. In this research topic, Yi Luan and Yu Zhang et al. discussed key MAMs-associated proteins and their functions in cardiovascular system and defined their roles in the progression of cardiac hypertrophy and heart failure (Luan et al.; Zhang et al.). Jiahao Zhao et al. showed the role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in CVDs (Zhao et al.). Importantly, the NLRP3 inflammasome has been shown to be influenced by MAMs to affect various cellular functions and, with it, CVDs (1).
Interactions between organelles can be involved in the progression of various cardiovascular diseases by influencing cell function (4). For example, MAMs mediated Ca2+ transport to mitochondria affects energy metabolism of cardiovascular cells, and is associated with myocardial hypertrophy, phenotypic changes and proliferation of VSMCs (5). MAMs mediated calcium flow also induces hypertrophic signal transduction and contraction responses; MAMs also induce endoplasmic reticulum and mitochondria-related cellular processes, such as ER stress and apoptosis, by regulating lipid and calcium ion transfer (6). MAMs recruit key signaling molecules and effector proteins as platforms for dynamic changes in inflammasome and mitochondria (1). Multiple studies have demonstrated that MAMs mediated mitochondrial function changes have occurred in the early stages of cardiovascular disease. Therefore, intervention for MAMs at the early stage of CVDs is also a new idea to treat CVDs.
Understanding the regulatory mechanisms and targeting proteins of MAMs integrity maintenance is important to explore new therapeutic targets for the prevention or treatment of heart-related diseases. For example, fluvoxamine has been used to treat heart failure and cardiac dysfunction in mouse and rat models of transverse aortic contraction due to its high affinity for Sig1R (7). Acetylcysteine, moreover, as a kind of antioxidant, is used in the treatment of mitochondrial damage and muscle dysfunction, this suggests that ROS are involved (8).
This research topic describes in detail the function of MAMs structure and its important role in cardiovascular diseases. On the one hand, MAMs maintain cell homeostasis and play a protective role by promoting mitochondrial division and mitochondrial autophagy; on the other hand, the increase of MAMs structure causes excessive mitochondrial division, mitochondrial calcium overload or oxidative stress. It causes pathological damage to cells. However, there are still many questions worth studying, such as whether the regulation effect of MAMs on cell function is similar in different tissues and conditions. What are the key molecules that maintain the structure and function of MAMs and how? Do mitochondria also influence endoplasmic reticulum function through MAMs? In conclusion, understanding the mechanisms that regulate the formation of MAMs structures and identifying the functions of the proteins involved in MAMs structures will help to suggest new strategies for the prevention and treatment of cardiovascular diseases in the future.
Author contributions
All authors contributed to the article and approved the submitted version.
Acknowledgments
The authors gratefully acknowledge the support of Frontiers in Cardiovascular Medicine staff for the continuous and passionate technical support.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Keywords: CVDs (Cardio vascular diseases), mitochondria, endoplasmic recticulum, ROS, mitochondria-associated endoplasmic reticulum membranes
Citation: Yang Y and Luan Y (2023) Editorial: Recent advances in mitochondria-associated endoplasmic reticulum membranes (MAMs) in heart-related diseases. Front. Cardiovasc. Med. 10:1168152. doi: 10.3389/fcvm.2023.1168152
Received: 17 February 2023; Accepted: 24 February 2023;
Published: 16 March 2023.
Edited and Reviewed by: Ichiro Manabe, Chiba University, Japan
© 2023 Yang and Luan. 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) and the copyright owner(s) 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: Yang Yang eWFuZ3lhbmdiaW9AMTYzLmNvbQ==
Specialty Section: This article was submitted to Cardiovascular Metabolism, a section of the journal Frontiers in Cardiovascular Medicine