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Endoplasmic reticulum-mitochondria crosstalk: from junction to function across neurological disorders.

Veeresh P1, Kaur H1, Sarmah D1,2, Mounica L1, Verma G1, Kotian V1, Kesharwani R1, Kalia K1, Borah A3, Wang X4, Dave KR5, Rodriguez AM2, Yavagal DR6, Bhattacharya P1.
Author information
1
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER) Ahmedabad, Gandhinagar, Gujarat, India.
2
Institut Mondor de Recherche Biomédicale (IMRB), INSERM U955, Université Paris-Est, UMR-S955, UPEC, Cretéil, France.
3
Cellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar, Assam, India.
4
Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
5
Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida.
6
Department of Neurology and Neurosurgery, University of Miami Miller School of Medicine, Miami, Florida.
Abstract
The endoplasmic reticulum (ER) and mitochondria are fundamental organelles highly interconnected with a specialized set of proteins in cells. ER-mitochondrial interconnections form specific microdomains, called mitochondria-associated ER membranes, that have been found to play important roles in calcium signaling and lipid homeostasis, and more recently in mitochondrial dynamics, inflammation, and autophagy. It is not surprising that perturbations in ER-mitochondria connections can result in the progression of disease, especially neurological disorders; hence, their architecture and regulation are crucial in determining the fate of cells and disease. The molecular identity of the specialized proteins regulating ER-mitochondrial crosstalk remains unclear. Our discussion here describes the physical and functional crosstalk between these two dynamic organelles and emphasizes the outcome of altered ER-mitochondrial interconnections in neurological disorders.
© 2019 New York Academy of Sciences.

KEYWORDS:
Alzheimer's disease; ERMES; Huntington's disease; MAMs; Parkinson's disease; amyotrophic lateral sclerosis; cerebral ischemia
PMID: 31460675 DOI: 10.1111/nyas.14212

Publication type, Grant support
Publication type
Review
Grant support
SB/YS/LS-196/2014/Department of Science and Technology (DST), Government of India/
Department of Pharmaceuticals, Ministry of Chemical and Fertilizers, Government of India/
National Institute of Pharmaceutical Education and Research/
International Society for Neurochemistry/

https://www.ncbi.nlm.nih.gov/pubmed/31460675