Mitochondrial fission and autophagy in the normal and diseased heart

Myriam Iglewski; Joseph A. Hill; Sergio Lavandero; Beverly A. Rothermel

doi:10.1007/s11906-010-0147-x

Mitochondrial fission and autophagy in the normal and diseased heart

Myriam Iglewski, Joseph A. Hill, Sergio Lavandero, Beverly A. Rothermel

Universidad de Chile

Research output: Contribution to journal › Review article › peer-review

59 Citations (Scopus)

Abstract

Sustained hypertension promotes structural, functional and metabolic remodeling of cardiomyocyte mitochondria. As long-lived, postmitotic cells, cardiomyocytes turn over mitochondria continuously to compensate for changes in energy demands and to remove damaged organelles. This process involves fusion and fission of existing mitochondria to generate new organelles and separate old ones for degradation via autophagy. Autophagy is a lysosome-dependent proteolytic pathway capable of processing cellular components, including organelles and protein aggregates. Autophagy can be either nonselective or selective and contributes to remodeling of the myocardium under stress. Fission of mitochondria, loss of membrane potential, and ubiquitination are emerging as critical steps that direct selective autophagic degradation of mitochondria. This review discusses the molecular mechanisms controlling mitochondrial dynamics, including fission, fusion, transport, and degradation. Furthermore, it examines recent studies revealing the importance of these processes in normal and diseased heart.

Original language	English
Pages (from-to)	418-425
Number of pages	8
Journal	Current Hypertension Reports
Volume	12
Issue number	6
DOIs	https://doi.org/10.1007/s11906-010-0147-x
Publication status	Published - Dec 2010

Bibliographical note

Funding Information:
Acknowledgments This research was funded in part by the National Institutes of Health (to J.A.H. and B.A.R.), the American Heart Association (to M.I., J.A.H., and B.A.R.), the American Heart Association-Jon Holden DeHaan Foundation (to J.A.H.), FONDECYT 1080436 (to S.L.), and FONDAP 1501006 (to S.L).

Funding

Acknowledgments This research was funded in part by the National Institutes of Health (to J.A.H. and B.A.R.), the American Heart Association (to M.I., J.A.H., and B.A.R.), the American Heart Association-Jon Holden DeHaan Foundation (to J.A.H.), FONDECYT 1080436 (to S.L.), and FONDAP 1501006 (to S.L).

Funders	Funder number
American Heart Association-Jon Holden DeHaan Foundation
National Institutes of Health
National Heart, Lung, and Blood Institute	R01HL072016
American Heart Association
Fondo Nacional de Desarrollo Científico y Tecnológico	1080436
Fondo de Financiamiento de Centros de Investigación en Áreas Prioritarias	1501006

ASJC Scopus Subject Areas

Internal Medicine

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10.1007/s11906-010-0147-x

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title = "Mitochondrial fission and autophagy in the normal and diseased heart",

abstract = "Sustained hypertension promotes structural, functional and metabolic remodeling of cardiomyocyte mitochondria. As long-lived, postmitotic cells, cardiomyocytes turn over mitochondria continuously to compensate for changes in energy demands and to remove damaged organelles. This process involves fusion and fission of existing mitochondria to generate new organelles and separate old ones for degradation via autophagy. Autophagy is a lysosome-dependent proteolytic pathway capable of processing cellular components, including organelles and protein aggregates. Autophagy can be either nonselective or selective and contributes to remodeling of the myocardium under stress. Fission of mitochondria, loss of membrane potential, and ubiquitination are emerging as critical steps that direct selective autophagic degradation of mitochondria. This review discusses the molecular mechanisms controlling mitochondrial dynamics, including fission, fusion, transport, and degradation. Furthermore, it examines recent studies revealing the importance of these processes in normal and diseased heart.",

author = "Myriam Iglewski and Hill, {Joseph A.} and Sergio Lavandero and Rothermel, {Beverly A.}",

note = "Funding Information: Acknowledgments This research was funded in part by the National Institutes of Health (to J.A.H. and B.A.R.), the American Heart Association (to M.I., J.A.H., and B.A.R.), the American Heart Association-Jon Holden DeHaan Foundation (to J.A.H.), FONDECYT 1080436 (to S.L.), and FONDAP 1501006 (to S.L).",

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Mitochondrial fission and autophagy in the normal and diseased heart

Abstract

Bibliographical note

Funding

ASJC Scopus Subject Areas

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