eprintid: 1542522
rev_number: 38
eprint_status: archive
userid: 608
dir: disk0/01/54/25/22
datestamp: 2017-02-28 14:28:52
lastmod: 2021-12-13 02:45:42
status_changed: 2017-05-04 11:17:16
type: article
metadata_visibility: show
creators_name: Ong, SB
creators_name: Kalkhoran, SB
creators_name: Hernández-Reséndiz, S
creators_name: Samangouei, P
creators_name: Ong, SG
creators_name: Hausenloy, DJ
title: Mitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It!
ispublished: pub
divisions: UCL
divisions: B02
divisions: D14
divisions: GA2
keywords: Drp1, Ischemia/reperfusion injury, Mfn1, Mfn2, Mitochondrial fission, Mitochondrial fusion, Mitochondrial morphology, OPA1
note: © The Author(s) 2017.

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
abstract: Mitochondrial health is critically dependent on the ability of mitochondria to undergo changes in mitochondrial morphology, a process which is regulated by mitochondrial shaping proteins. Mitochondria undergo fission to generate fragmented discrete organelles, a process which is mediated by the mitochondrial fission proteins (Drp1, hFIS1, Mff and MiD49/51), and is required for cell division, and to remove damaged mitochondria by mitophagy. Mitochondria undergo fusion to form elongated interconnected networks, a process which is orchestrated by the mitochondrial fusion proteins (Mfn1, Mfn2 and OPA1), and which enables the replenishment of damaged mitochondrial DNA. In the adult heart, mitochondria are relatively static, are constrained in their movement, and are characteristically arranged into 3 distinct subpopulations based on their locality and function (subsarcolemmal, myofibrillar, and perinuclear). Although the mitochondria are arranged differently, emerging data supports a role for the mitochondrial shaping proteins in cardiac health and disease. Interestingly, in the adult heart, it appears that the pleiotropic effects of the mitochondrial fusion proteins, Mfn2 (endoplasmic reticulum-tethering, mitophagy) and OPA1 (cristae remodeling, regulation of apoptosis, and energy production) may play more important roles than their pro-fusion effects. In this review article, we provide an overview of the mitochondrial fusion and fission proteins in the adult heart, and highlight their roles as novel therapeutic targets for treating cardiac disease.
date: 2017-02-11
date_type: published
official_url: http://dx.doi.org/10.1007/s10557-016-6710-1
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 1210239
doi: 10.1007/s10557-016-6710-1
pii: 10.1007/s10557-016-6710-1
lyricists_name: Hausenloy, Derek
lyricists_id: DHAUS05
actors_name: Bracey, Alan
actors_id: ABBRA90
actors_role: owner
full_text_status: public
publication: Cardiovascular Drugs and Therapy
volume: 31
number: 1
pagerange: 87-107
event_location: United States
issn: 1573-7241
citation:        Ong, SB;    Kalkhoran, SB;    Hernández-Reséndiz, S;    Samangouei, P;    Ong, SG;    Hausenloy, DJ;      (2017)    Mitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It!                   Cardiovascular Drugs and Therapy , 31  (1)   pp. 87-107.    10.1007/s10557-016-6710-1 <https://doi.org/10.1007/s10557-016-6710-1>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/1542522/3/art%253A10.1007%252Fs10557-016-6710-1.pdf