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Updated: Mar 5, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Potential Roles of Mitochondria-Associated ER Membranes (MAMs) in Traumatic Brain Injury
Dongdong Sun1,2, Xin Chen3,4,5, Gang Gu1,2
1Department of Neurosurgery, Tianjin Medical University, General Hospital, Tianjin, People's Republic of China.
Abstract:
The endoplasmic reticulum (ER) and mitochondria have both been shown to be critical in cellular homeostasis. The functions of the ER and mitochondria are independent but interrelated. These two organelles could form physical interactions, known as MAMs, to regulate physiological functions between ER and mitochondria to maintain Ca2+, lipid, and metabolite exchange. Several proteins are located in MAMs, including RNA-dependent protein kinase (PKR)-like ER kinase, inositol 1,4,5-trisphosphate receptors, phosphofurin acidic cluster sorting protein-2 and sigma-1 receptor to ensure regulation. Recent studies indicated that MAMs participate in inflammation and apoptosis in various conditions. All of these functions are crucial in determining cell fate following traumatic brain injury (TBI). We hypothesized that MAMs may associate with TBI and could contribute to mitochondrial dysfunction, ER stress, autophagy dysregulation, dysregulation of Ca2+ homeostasis, and oxidative stress. In this review, we summarize the latest understanding of MAM formation and their potential regulatory role in TBI pathophysiology.
Insights
Mitochondria-associated membranes (MAMs) are crucial for cellular balance. This review explores MAMs
Area of Science:
- Cellular Biology
- Neuroscience
- Biochemistry
Background:
- The endoplasmic reticulum (ER) and mitochondria are vital organelles for cellular homeostasis.
- These organelles interact via mitochondria-associated membranes (MAMs) to regulate Ca2+, lipid, and metabolite exchange.
- MAMs involve key proteins like sigma-1 receptor and PKR-like ER kinase, influencing cellular functions.
Purpose of the Study:
- To review the formation of MAMs.
- To explore the potential role of MAMs in traumatic brain injury (TBI) pathophysiology.
- To understand how MAMs contribute to cellular dysfunction following TBI.
Main Methods:
- Literature review of recent studies on MAMs and TBI.
- Synthesis of current understanding of MAM formation and function.
- Analysis of MAMs' involvement in TBI-related cellular processes.
Main Results:
- MAMs are implicated in inflammation and apoptosis.
- MAMs are hypothesized to associate with TBI.
- MAMs may contribute to mitochondrial dysfunction, ER stress, and altered Ca2+ homeostasis in TBI.
Conclusions:
- MAMs play a significant role in cellular homeostasis.
- Dysregulation of MAMs is likely involved in TBI.
- Further research into MAMs could reveal new therapeutic targets for TBI.
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