IP3 receptor trafficking at the ER-mitochondria contacts impacts on mitochondrial Ca2+ homeostasis and metabolism

Karim Rahhali; Fabio Di Lisa; Nina Kaludercic

doi:10.1016/j.ceca.2023.102700

IP₃ receptor trafficking at the ER-mitochondria contacts impacts on mitochondrial Ca²⁺ homeostasis and metabolism

Cell Calcium. 2023 Mar:110:102700. doi: 10.1016/j.ceca.2023.102700. Epub 2023 Jan 25.

Authors

Karim Rahhali¹, Fabio Di Lisa², Nina Kaludercic³

Affiliations

¹ Department of Biomedical Sciences, University of Padova, Italy.
² Department of Biomedical Sciences, University of Padova, Italy; Neuroscience Institute, National Research Council of Italy (CNR), Italy.
³ Department of Biomedical Sciences, University of Padova, Italy; Neuroscience Institute, National Research Council of Italy (CNR), Italy; Fondazione Istituto di Ricerca Pediatrica Città della Speranza (IRP), Italy. Electronic address: nina.kaludercic@unipd.it.

PMID: 36716521
DOI: 10.1016/j.ceca.2023.102700

Abstract

The close contacts between endoplasmic reticulum and mitochondria (ERMCs) play a key role in metabolic regulation, Ca²⁺ homeostasis, reactive oxygen species production, and many other cell functions. Nevertheless, it is not fully clear how these contacts dynamically rearrange to support cell functions. In a recent Nature Communications article [1], Katona et al. elegantly showed that motile IP₃Rs can be captured at ERMCs to promptly mediate Ca²⁺ transfer and stimulate mitochondrial oxidative metabolism.

Keywords: Contact sites; Endoplasmic reticulum; IP(3) receptor; Mitochondria.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Calcium / metabolism
Calcium Signaling* / physiology
Homeostasis / physiology
Mitochondria* / metabolism

Substances

Calcium