Mitochondria‐associated endoplasmic reticulum membrane: Overview and inextricable link with cancer

Yang, Xi; Jing, Zhuang; Song, Wei; Shen, Wangjie; Wu, Wei; Shen, Hong; Han, Shuwen

doi:10.1111/jcmm.17696

Cited by 18 publications

(9 citation statements)

References 161 publications

(280 reference statements)

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“…Differently from MFN1, a small fraction of MFN2 has been observed to be located in ER membranes juxtaposed to outer mitochondrial membranes. MFN2 deletion is reported to induce an ER stress, through a mechanism still under debate (Yang et al., 2023), which can lead to a deterioration of cellular functions (Filadi et al., 2018).…”

Section: Cell Metabolism Correlates With Mitochondrial Morphodynamicsmentioning

confidence: 99%

Mitochondria: At the crossroads between mechanobiology and cell metabolism

Villard

Manneville

2023

Biology of the Cell

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Metabolism and mechanics are two key facets of structural and functional processes in cells, such as growth, proliferation, homeostasis and regeneration. Their reciprocal regulation has been increasingly acknowledged in recent years: external physical and mechanical cues entail metabolic changes, which in return regulate cell mechanosensing and mechanotransduction. Since mitochondria are pivotal regulators of metabolism, we review here the reciprocal links between mitochondrial morphodynamics, mechanics and metabolism. Mitochondria are highly dynamic organelles which sense and integrate mechanical, physical and metabolic cues to adapt their morphology, the organization of their network and their metabolic functions. While some of the links between mitochondrial morphodynamics, mechanics and metabolism are already well established, others are still poorly documented and open new fields of research. First, cell metabolism is known to correlate with mitochondrial morphodynamics. For instance, mitochondrial fission, fusion and cristae remodeling allow the cell to fine‐tune its energy production through the contribution of mitochondrial oxidative phosphorylation and cytosolic glycolysis. Second, mechanical cues and alterations in mitochondrial mechanical properties reshape and reorganize the mitochondrial network. Mitochondrial membrane tension emerges as a decisive physical property which regulates mitochondrial morphodynamics. However, the converse link hypothesizing a contribution of morphodynamics to mitochondria mechanics and/or mechanosensitivity has not yet been demonstrated. Third, we highlight that mitochondrial mechanics and metabolism are reciprocally regulated, although little is known about the mechanical adaptation of mitochondria in response to metabolic cues. Deciphering the links between mitochondrial morphodynamics, mechanics and metabolism still presents significant technical and conceptual challenges but is crucial both for a better understanding of mechanobiology and for potential novel therapeutic approaches in diseases such as cancer.

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Section: Cell Metabolism Correlates With Mitochondrial Morphodynamicsmentioning

confidence: 99%

Mitochondria: At the crossroads between mechanobiology and cell metabolism

Villard

Manneville

2023

Biology of the Cell

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“…The ER and mitochondria play crucial roles in regulating cellular homeostasis and cell death, especially cross-talk of these organelles mediated by Calcium ion are important for survival of cancer cells [ 34 ]. The link between induction of ROS, activation of the ER stress pathway, and apoptotic death has been demonstrated in various cancer cell lines by various natural compounds [ 35 , 36 , 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Shikonin Induces ROS-Dependent Apoptosis Via Mitochondria Depolarization and ER Stress in Adult T Cell Leukemia/Lymphoma

2023

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Adult T cell leukemia/lymphoma (ATLL) is an aggressive T-cell malignancy that develops in some elderly human T-cell leukemia virus (HTVL-1) carriers. ATLL has a poor prognosis despite conventional and targeted therapies, and a new safe and efficient therapy is required. Here, we examined the anti-ATLL effect of Shikonin (SHK), a naphthoquinone derivative that has shown several anti-cancer activities. SHK induced apoptosis of ATLL cells accompanied by generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential, and induction of endoplasmic reticulum (ER) stress. Treatment with a ROS scavenger, N-acetylcysteine (NAC), blocked both loss of mitochondrial membrane potential and ER stress, and prevented apoptosis of ATLL cells, indicating that ROS is an upstream trigger of SHK-induced apoptosis of ATLL cells through disruption of the mitochondrial membrane potential and ER stress. In an ATLL xenografted mouse model, SHK treatment suppressed tumor growth without significant adverse effects. These results suggest that SHK could be a potent anti-reagent against ATLL.

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“…During ER stress, IRE1 interacts with Sig-1R to promote dimerization. As a calcium receptor, when ER calcium is depleted, Sig-1R dissociates from GRP78, thereby promoting the transfer of calcium to mitochondria through IP3R [ 84 ]. Previous studies have demonstrated that PERK is abundantly present in the ER and MAM in high glucose-cultured cardiomyocytes.…”

Section: Er Stressmentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment

Liu,

Huo,

Ren

et al. 2024

Cell Death Discov.

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Diabetic cardiomyopathy (DCM), an important complication of diabetes mellitus (DM), is one of the most serious chronic heart diseases and has become a major cause of heart failure worldwide. At present, the pathogenesis of DCM is unclear, and there is still a lack of effective therapeutics. Previous studies have shown that the homeostasis of mitochondria and the endoplasmic reticulum (ER) play a core role in maintaining cardiovascular function, and structural and functional abnormalities in these organelles seriously impact the occurrence and development of various cardiovascular diseases, including DCM. The interplay between mitochondria and the ER is mediated by the mitochondria-associated ER membrane (MAM), which participates in regulating energy metabolism, calcium homeostasis, mitochondrial dynamics, autophagy, ER stress, inflammation, and other cellular processes. Recent studies have proven that MAM is closely related to the initiation and progression of DCM. In this study, we aim to summarize the recent research progress on MAM, elaborate on the key role of MAM in DCM, and discuss the potential of MAM as an important therapeutic target for DCM, thereby providing a theoretical reference for basic and clinical studies of DCM treatment.

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Mitochondria‐associated endoplasmic reticulum membrane: Overview and inextricable link with cancer

Cited by 18 publications

References 161 publications

Mitochondria: At the crossroads between mechanobiology and cell metabolism

Mitochondria: At the crossroads between mechanobiology and cell metabolism

Shikonin Induces ROS-Dependent Apoptosis Via Mitochondria Depolarization and ER Stress in Adult T Cell Leukemia/Lymphoma

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment

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