Compositions and Functions of Mitochondria-Associated Endoplasmic Reticulum Membranes and Their Contribution to Cardioprotection by Exercise Preconditioning

Lv, Yuhu; Cheng, Lin; Peng, Fenglin

doi:10.3389/fphys.2022.910452

Cited by 10 publications

(11 citation statements)

References 146 publications

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“…This approach enables the potential for extended treatment of tumors. In addition, it should be noted that exercise preconditioning has the potential to regulate MAMs, which may contribute to a protective effect on the heart ( Lv et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Ding,

Liu,

Zhang

et al. 2024

Front. Pharmacol.

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Cardiovascular diseases (CVDs) are currently the leading cause of death worldwide. In 2022, the CVDs contributed to 19.8 million deaths globally, accounting for one-third of all global deaths. With an aging population and changing lifestyles, CVDs pose a major threat to human health. Mitochondria-associated endoplasmic reticulum membranes (MAMs) are communication platforms between cellular organelles and regulate cellular physiological functions, including apoptosis, autophagy, and programmed necrosis. Further research has shown that MAMs play a critical role in the pathogenesis of CVDs, including myocardial ischemia and reperfusion injury, heart failure, pulmonary hypertension, and coronary atherosclerosis. This suggests that MAMs could be an important therapeutic target for managing CVDs. The goal of this study is to summarize the protein complex of MAMs, discuss its role in the pathological mechanisms of CVDs in terms of its functions such as Ca2+ transport, apoptotic signaling, and lipid metabolism, and suggest the possibility of MAMs as a potential therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Ding,

Liu,

Zhang

et al. 2024

Front. Pharmacol.

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“…Also relevant to mitochondrial function, hypoxia, which is a feature of AD [ 215 ], upregulates BACE1 at the transcriptional level [ 216 ]. Given this multiplicity of functions, it is highly likely that MAM composition, not only its constituent proteins and lipids, but even microRNAs [ 217 ], differs in different cell types, at different times, and in response to different environments [ 218 ].…”

Section: Mam: a Lipid Raft In The Ermentioning

confidence: 99%

Towards a Unitary Hypothesis of Alzheimer’s Disease Pathogenesis

Area-Gomez,

Schon

2024

JAD

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The “amyloid cascade” hypothesis of Alzheimer’s disease (AD) pathogenesis invokes the accumulation in the brain of plaques (containing the amyloid-β protein precursor [AβPP] cleavage product amyloid-β [Aβ]) and tangles (containing hyperphosphorylated tau) as drivers of pathogenesis. However, the poor track record of clinical trials based on this hypothesis suggests that the accumulation of these peptides is not the only cause of AD. Here, an alternative hypothesis is proposed in which the AβPP cleavage product C99, not Aβ, is the main culprit, via its role as a regulator of cholesterol metabolism. C99, which is a cholesterol sensor, promotes the formation of mitochondria-associated endoplasmic reticulum (ER) membranes (MAM), a cholesterol-rich lipid raft-like subdomain of the ER that communicates, both physically and biochemically, with mitochondria. We propose that in early-onset AD (EOAD), MAM-localized C99 is elevated above normal levels, resulting in increased transport of cholesterol from the plasma membrane to membranes of intracellular organelles, such as ER/endosomes, thereby upregulating MAM function and driving pathology. By the same token, late-onset AD (LOAD) is triggered by any genetic variant that increases the accumulation of intracellular cholesterol that, in turn, boosts the levels of C99 and again upregulates MAM function. Thus, the functional cause of AD is upregulated MAM function that, in turn, causes the hallmark disease phenotypes, including the plaques and tangles. Accordingly, the MAM hypothesis invokes two key interrelated elements, C99 and cholesterol, that converge at the MAM to drive AD pathogenesis. From this perspective, AD is, at bottom, a lipid disorder.

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“…Emerging evidence suggests that exercise, or exercise preconditioning (EP), potentially contributes to cardiac protection by modulating MAM proteins and functions ( 84 ). For instance, EP exerts its protective effects by regulating various molecules, including MFN2, MFN1, FUNDC1, VDAC1, GRP75, IP3R, CYPD, and others, all impacting MAM function.…”

Section: Role Of Mam In Cardiac Diseasementioning

confidence: 99%

So close, yet so far away: the relationship between MAM and cardiac disease

Lu,

Chen,

et al. 2024

Front. Cardiovasc. Med.

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Mitochondria-associated membrane (MAM) serve as crucial contact sites between mitochondria and the endoplasmic reticulum (ER). Recent research has highlighted the significance of MAM, which serve as a platform for various protein molecules, in processes such as calcium signaling, ATP production, mitochondrial structure and function, and autophagy. Cardiac diseases caused by any reason can lead to changes in myocardial structure and function, significantly impacting human health. Notably, MAM exhibits various regulatory effects to maintain cellular balance in several cardiac diseases conditions, such as obesity, diabetes mellitus, and cardiotoxicity. MAM proteins independently or interact with their counterparts, forming essential tethers between the ER and mitochondria in cardiomyocytes. This review provides an overview of key MAM regulators, detailing their structure and functions. Additionally, it explores the connection between MAM and various cardiac injuries, suggesting that precise genetic, pharmacological, and physical regulation of MAM may be a promising strategy for preventing and treating heart failure.

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Compositions and Functions of Mitochondria-Associated Endoplasmic Reticulum Membranes and Their Contribution to Cardioprotection by Exercise Preconditioning

Cited by 10 publications

References 146 publications

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Towards a Unitary Hypothesis of Alzheimer’s Disease Pathogenesis

So close, yet so far away: the relationship between MAM and cardiac disease

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