Calcium transfer between endoplasmic reticulum and mitochondria in liver diseases

Jin, Chaonan; Kumar, Pranav; Gracia‐Sancho, Jordi; Dufour, Jean‐François

doi:10.1002/1873-3468.14078

Cited by 17 publications

(6 citation statements)

References 96 publications

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“…In addition, oncogenes and tumor suppressor proteins can play other roles in cancer development through Ca 2+ signal regulation, such as resistance to apoptosis. Because mitochondrial Ca 2+ overload is related to apoptosis and death, modifying ER−mitochondria Ca 2+ transfer at the MAM will change the sensitivity of apoptosis, and tumor cells can acquire resistance to cell death accordingly [ 136 ]. For example, by inhibiting IP 3 R-mediated Ca 2+ signaling or increasing the transmembrane distance at the MAM, the efficiency of ER−mitochondria Ca 2+ transfer can be reduced, so as to decrease the sensitivity of tumor cells to apoptosis [ 137 ] ( Figure 4 ).…”

Section: Mitochondrial Ca 2+ and Tumor Cell Apoptosismentioning

confidence: 99%

The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

Zhang

et al. 2022

IJMS

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Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca2+ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca2+ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca2+ in both mitochondria and cytoplasm, thereby regulating cellular Ca2+ homeostasis. Mitochondrial Ca2+ transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca2+ homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca2+ and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca2+ regulation helps diagnosis and therapy.

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Section: Mitochondrial Ca 2+ and Tumor Cell Apoptosismentioning

confidence: 99%

The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

Zhang

et al. 2022

IJMS

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“…The Ca 2+ released from ER can be efficiently transferred to mitochondria, resulting in mitochondrial Ca 2+ overload, a key factor in the opening of mitochondrial permeability transition pores to increase mitochondrial ROS production and reduce ATP production. 46,47 High Ca 2+ levels and the subsequent loss of the MMP initiated the intrinsic apoptosis pathway. Tsai et al 48 have shown that graphene can lead to the release of Ca 2+ from ER and then activate the mitochondria-dependent apoptosis signaling pathway.…”

Section: And S3-s19 †)mentioning

confidence: 99%

Cytotoxicity and RNA-sequencing analysis of macrophages after exposure to vanadium dioxide nanoparticles

Tang

et al. 2022

Environ. Sci.: Nano

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“…Recent studies have shown that the regulation of ERMCs and mitochondrial dynamics are two closely intertwined processes ( Friedman et al, 2011 ). Studies have shown that the sites of MAMs in rat heart cells coincide with the outer mitochondrial membrane (OMM) – inner mitochondrial membrane (IMM) contact sites, and therefore, MAMs may form calcium channel complexes to regulate Ca 2+ transport between the endoplasmic reticulum and mitochondria ( Jin et al, 2021 ). The inositol 1,4,5-triphosphate receptor (IP3R) is located in the ER membrane and regulates Ca 2+ release, and voltage-dependent anion selective channel protein (VDAC) 1 is a Ca 2+ uptake channel on the OMM ( Szabadkai et al, 2006 ).…”

Section: Structure Of Endoplasmic Reticulum-mitochondria Contactsmentioning

confidence: 99%

Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

Wang

Zhang

Wen

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular remodeling occurs in cardiomyocytes, collagen meshes, and vascular beds in the progress of cardiac insufficiency caused by a variety of cardiac diseases such as chronic ischemic heart disease, chronic overload heart disease, myocarditis, and myocardial infarction. The morphological changes that occur as a result of remodeling are the critical pathological basis for the occurrence and development of serious diseases and also determine morbidity and mortality. Therefore, the inhibition of remodeling is an important approach to prevent and treat heart failure and other related diseases. The endoplasmic reticulum (ER) and mitochondria are tightly linked by ER-mitochondria contacts (ERMCs). ERMCs play a vital role in different signaling pathways and provide a satisfactory structural platform for the ER and mitochondria to interact and maintain the normal function of cells, mainly by involving various cellular life processes such as lipid metabolism, calcium homeostasis, mitochondrial function, ER stress, and autophagy. Studies have shown that abnormal ERMCs may promote the occurrence and development of remodeling and participate in the formation of a variety of cardiovascular remodeling-associated diseases. This review focuses on the structure and function of the ERMCs, and the potential mechanism of ERMCs involved in cardiovascular remodeling, indicating that ERMCs may be a potential target for new therapeutic strategies against cardiovascular remodeling-induced diseases.

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Calcium transfer between endoplasmic reticulum and mitochondria in liver diseases

Cited by 17 publications

References 96 publications

The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

Cytotoxicity and RNA-sequencing analysis of macrophages after exposure to vanadium dioxide nanoparticles

Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

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