Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes

Both iron overload and deficiency can promote development of cardiomyopathy. Advances in our knowledge from recent research have indicated numerous potential cellular mechanisms. Regulation of myocardial autophagy by iron is of particular interest and will be reviewed here. Autophagy is already well...

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Main Authors: Eddie Tam, Chloe Reno, Khang Nguyen, Sungji Cho, Gary Sweeney
Format: Article
Language:English
Published: IMR Press 2022-05-01
Series:Reviews in Cardiovascular Medicine
Subjects:
Online Access:https://www.imrpress.com/journal/RCM/23/5/10.31083/j.rcm2305167
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author Eddie Tam
Chloe Reno
Khang Nguyen
Sungji Cho
Gary Sweeney
author_facet Eddie Tam
Chloe Reno
Khang Nguyen
Sungji Cho
Gary Sweeney
author_sort Eddie Tam
collection DOAJ
description Both iron overload and deficiency can promote development of cardiomyopathy. Advances in our knowledge from recent research have indicated numerous potential cellular mechanisms. Regulation of myocardial autophagy by iron is of particular interest and will be reviewed here. Autophagy is already well established to play a significant role in regulating the development of heart failure. This review will focus on regulation of autophagy by iron, crosstalk between autophagy and other cellular process which have also already been implicated in heart failure (oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, ferroptosis) and the therapeutic potential of targeting these interactions.
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spelling doaj.art-9efb8bd894d44dda8477b87797af876b2022-12-22T02:29:07ZengIMR PressReviews in Cardiovascular Medicine1530-65502022-05-0123516710.31083/j.rcm2305167S1530-6550(22)00500-2Importance of Autophagy in Mediating Cellular Responses to Iron Overload in CardiomyocytesEddie Tam0Chloe Reno1Khang Nguyen2Sungji Cho3Gary Sweeney4Department of Biology, York University, Toronto, ON M3J 1P3, CanadaDepartment of Biology, York University, Toronto, ON M3J 1P3, CanadaDepartment of Biology, York University, Toronto, ON M3J 1P3, CanadaDepartment of Biology, York University, Toronto, ON M3J 1P3, CanadaDepartment of Biology, York University, Toronto, ON M3J 1P3, CanadaBoth iron overload and deficiency can promote development of cardiomyopathy. Advances in our knowledge from recent research have indicated numerous potential cellular mechanisms. Regulation of myocardial autophagy by iron is of particular interest and will be reviewed here. Autophagy is already well established to play a significant role in regulating the development of heart failure. This review will focus on regulation of autophagy by iron, crosstalk between autophagy and other cellular process which have also already been implicated in heart failure (oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, ferroptosis) and the therapeutic potential of targeting these interactions.https://www.imrpress.com/journal/RCM/23/5/10.31083/j.rcm2305167iron overloadautophagyadiponectinoxidative stressendoplasmic reticulum stressmitochondriaferroptosis
spellingShingle Eddie Tam
Chloe Reno
Khang Nguyen
Sungji Cho
Gary Sweeney
Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
Reviews in Cardiovascular Medicine
iron overload
autophagy
adiponectin
oxidative stress
endoplasmic reticulum stress
mitochondria
ferroptosis
title Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
title_full Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
title_fullStr Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
title_full_unstemmed Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
title_short Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes
title_sort importance of autophagy in mediating cellular responses to iron overload in cardiomyocytes
topic iron overload
autophagy
adiponectin
oxidative stress
endoplasmic reticulum stress
mitochondria
ferroptosis
url https://www.imrpress.com/journal/RCM/23/5/10.31083/j.rcm2305167
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