REVIEW article
Front. Cell Dev. Biol.
Sec. Signaling
Role of Mitochondria-Associated Membranes (MAMs) in Inflammatory Signaling: Implications for Acute Lung Injury Pathogenesis
Provisionally accepted
- Shaoxing Second Hospital, Shaoxing, China
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Mitochondria-associated membranes (MAMs), the specialized contact regions linking the endoplasmic reticulum (ER) and mitochondria, have emerged as dynamic communication hubs critical for preserving cellular homeostasis. These structures are crucial for controlling a range of essential cellular processes, such as calcium (Ca2+) signaling, lipid metabolism, autophagy, apoptosis, and inflammatory response. Increasing evidence connects MAM dysfunction to various inflammatory conditions, such as metabolic disorders, neurodegenerative diseases, and antiviral response. In the context of acute lung injury, altered ER–mitochondria interactions can result in mitochondria Ca2+ overload, heightened oxidative stress, and augmented inflammatory response. Together, these pathological processes enhance endothelial permeability and exacerbate pulmonary inflammation. This review highlights the structural and functional attributes of MAMs, the mechanisms underlying MAM-mediated inflammation, and the roles of MAMs in metabolic, neurological, and antiviral inflammation. It also delves into the role of MAMs in acute lung injury, unveiling fresh insights that may pave the way for innovative therapies targeting ER–mitochondria crosstalk.
Keywords: mitochondria-associated membranes (MAMs), Mitochondria, Endoplasmic Reticulum, Inflammation, Acute Lung Injury
Received: 22 Aug 2025; Accepted: 04 Nov 2025.
Copyright: © 2025 Qian, Qiu, Xu and Zheng. 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: Guoping Zheng, zgp28037@163.com
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