Article
Biochemistry & Molecular Biology
Chaonan Jin, Eric Felli, Naomi Franziska Lange, Annalisa Berzigotti, Jordi Gracia-Sancho, Jean-Francois Dufour
Summary: The interaction between the mitochondria and the endoplasmic reticulum (ER) plays a crucial role in hepatocyte function. The abundance of ER-mitochondria contacts (ERMCs) is associated with the severity of non-alcoholic fatty liver disease (NAFLD) and its progression to non-alcoholic steatohepatitis (NASH). The density of ERMCs increases with the number of metabolic syndrome (MetS) features, suggesting a role for this interaction in the pathophysiology of NASH.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Na Song, Ming Yang, Hao Zhang, Shi-kun Yang
Summary: Kidney disease is a serious health concern, and understanding the pathogenesis is crucial for precise therapies. Disruption of calcium homeostasis plays a fundamental role in kidney disease development and is a promising therapeutic strategy. The endoplasmic reticulum and mitochondria are key organelles, with pharmacologic modulation of cellular calcium homeostasis as a novel treatment approach.
CURRENT MEDICINAL CHEMISTRY
(2021)
Article
Biochemistry & Molecular Biology
Leonora Szabo, Nadia Cummins, Paolo Paganetti, Alex Odermatt, Andreas Papassotiropoulos, Celeste Karch, Jurgen Gotz, Anne Eckert, Amandine Grimm
Summary: Abnormal tau protein disrupts the interaction between the endoplasmic reticulum (ER) and mitochondria, leading to impaired mitochondrial function and cholesterol metabolism. This study shows that abnormal tau loosens the association between ER and mitochondria, particularly through the VAPB-PTPIP51 pathway. Disruption of the ER-mitochondria interaction results in altered levels of mitochondrial cholesterol and pregnenolone, which can be restored by inhibiting GSK3 beta.
Article
Biochemistry & Molecular Biology
Mengzhen Yue, Bing Hu, Jiajia Li, Ruifeng Chen, Zhen Yuan, Hurong Xiao, Haishuang Chang, Yaming Jiu, Kun Cai, Binbin Ding
Summary: The coronavirus ORF6 protein targets lipid droplets, localizes to the mitochondria-LD and ER-LD contact sites, and regulates LD biogenesis and lipolysis. It interacts with ER membrane proteins BAP31 and USE1 to mediate ER-LDs contact formation and links the SAM complex in the mitochondrial outer membrane to LDs. ORF6 promotes cellular lipolysis and LD biogenesis to reprogram host cell lipid flux and facilitate viral production.
Review
Cell Biology
Yu Wang, Xinrong Zhang, Ya Wen, Sixuan Li, Xiaohui Lu, Ran Xu, Chao Li
Summary: Cardiovascular remodeling is a critical pathological basis for heart failure caused by various cardiac diseases, affecting morbidity and mortality. The ER and mitochondria are connected by ERMCs, playing a key role in cellular processes and potentially contributing to cardiovascular remodeling-associated diseases. Ongoing research suggests that targeting ERMCs may offer new therapeutic strategies against diseases induced by cardiovascular remodeling.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Cell Biology
Kihyoun Park, Myung-Shik Lee
Summary: Autophagy plays a crucial role in maintaining organelle function and intracellular nutrient balance. Dysregulated autophagy is implicated in various diseases, including metabolic disorders, neurodegenerative diseases, infections, and cardiovascular diseases. Research is underway to find autophagy modulators for the treatment of these diseases and it is expected that authentic autophagy modulators will be developed in the near future.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Masahiro Kawahara, Ken-ichiro Tanaka, Midori Kato-Negishi
Summary: Copper is an essential trace element that plays critical roles in brain functions, working alongside zinc to modulate neuronal transmission at synapses for information processing. However, low concentrations of copper during transient global ischemia exacerbate zinc-induced neurotoxicity, leading to ER stress, SAPK/JNK pathway activation, and increased ROS production. The collaborative roles of copper in zinc-induced neurotoxicity at synapses and its contribution to the pathogenesis of vascular dementia are significant topics for further research.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Cell Biology
Pablo Morgado-Caceres, Gianella Liabeuf, Ximena Calle, Lautaro Briones, Jaime A. Riquelme, Roberto Bravo-Sagua, Valentina Parra
Summary: The complex physiology of eukaryotic cells relies on the interaction between organelles, and the mitochondria-endoplasmic reticulum contacts (MERCs) play a crucial role in calcium and lipid transfer as well as other subcellular processes. MERCs are dynamic structures that can remodel according to cellular cues, adjusting the function of organelles. Dysfunction of MERCs is associated with the development of age-related disorders.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Review
Cell Biology
Vishwadeep Shelke, Vinayak Yelgonde, Ajinath Kale, Maciej Lech, Anil Bhanudas Gaikwad
Summary: Kidney diseases affect over 800 million individuals worldwide and demand increased efforts in prevention and treatment. The complex pathophysiology of kidney diseases involves dysfunctions in various organelles, such as mitochondria and endoplasmic reticulum. Recent findings demonstrate interactions between the endoplasmic reticulum and other cell compartments, shedding light on cellular mechanisms in health and disease. The regulation of organelle dynamics by epigenetic mechanisms, including DNA methylation and noncoding RNAs, may offer potential therapeutic targets against kidney diseases.
JOURNAL OF CELLULAR PHYSIOLOGY
(2023)
Article
Cell Biology
Yuan Che, Wanfen Xu, Chujie Ding, Tianyu He, Xiaowei Xu, Yubing Shuai, Hai Huang, Jiawei Wu, Yun Wang, Chen Wang, Guangji Wang, Lijuan Cao, Haiping Hao
Summary: Bile acids serve as endogenous ligands of mitofusin 2 (MFN2) and regulate innate immune response to bacterial infection under cholestatic and physiological conditions. At high concentrations, bile acids promote the activation of NLRP3 inflammasome and pyroptosis, while at physiologically relevant low concentrations, they enhance mitochondrial fusion and strengthen macrophage-mediated phagocytotic clearance. These findings highlight the important role of bile acids as activators of MFN2 in shaping innate immune responses against infections, connecting systemic metabolism with mitochondrial dynamics.
Editorial Material
Biochemistry & Molecular Biology
Emma Burbridge, Colin Adrain
Summary: This article discusses the importance and mechanisms of maintaining organelle homeostasis in cells, providing a comprehensive perspective on the functions and interactions of various organelles. It also introduces some lesser-known organelles.
Review
Cell Biology
Junsheng Chen, Arthur Bassot, Fabrizio Giuliani, Thomas Simmen
Summary: ALS is a devastating neurodegenerative disease without cure, with a potential involvement of dysfunctional mitochondria-endoplasmic reticulum contacts (MERCs) leading to altered mitochondrial bioenergetics and oxidative stress. VAPB and VCP are key players in ALS pathogenesis, interacting with other mutant proteins and causing ER stress, inflammation, and motor neuron death. The dysfunction of MERCs in ALS triggers a cascade of pathological changes in the cell.
Article
Biochemistry & Molecular Biology
Jingjing Pan, Yanfeng Wei, Linlin Ni, Xiaoyang Li, Yu Deng, Bin Xu, Tianyao Yang, Jingyi Sun, Wei Liu
Summary: This study investigates the role of calcium ion (Ca2+) homeostasis in MeHg-induced neurotoxicity. The results suggest that MeHg causes cell damage and increases Ca2+ release from the ER as well as free Ca2+ levels in the cytoplasm and mitochondria. Ca2+ channel inhibitors and Ca2+ chelator can partially inhibit MeHg-induced mitochondrial damage and apoptosis.
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
(2022)
Article
Biology
Dorian V. Ziegler, Nadine Martin, David Bernard
Summary: The study explores the impact of mitochondria-endoplasmic reticulum contacts (MERCs) biology on cellular senescence and its relation to age-related diseases. It discusses the modulation of aging by MERCs and their role in regulating cellular senescence, potentially contributing to the aging process.
COMMUNICATIONS BIOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Barbara Zablocka, Dariusz C. Gorecki, Krzysztof Zablocki
Summary: Duchenne muscular dystrophy is caused by mutations in the DMD gene, leading to the loss of full-length dystrophin and resulting in muscle degeneration, neuropsychological impairment, and bone deformities. Abnormalities in calcium homeostasis are a common feature of this disease, playing a fundamental role in the various abnormalities associated with DMD.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)