Ferritinophagy and ferroptosis in the management of metabolic diseases

Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for tar...

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Published in:	TRENDS IN ENDOCRINOLOGY AND METABOLISM Vol. 32; no. 7; pp. 444 - 462
Main Authors:	Ajoolabady, Amir, Aslkhodapasandhokmabad, Hamid, Libby, Peter, Tuomilehto, Jaakko, Lip, Gregory Y.H., Penninger, Josef M., Richardson, Des R., Tang, Daolin, Zhou, Hao, Wang, Shuyi, Klionsky, Daniel J., Kroemer, Guido, Ren, Jun
Format:	Journal Article Publication
Language:	English
Published:	United States Elsevier Ltd 01.07.2021
Subjects:	Autophagy Endocrinology and Metabolism ferritinophagy Ferritins Ferroptosis Humans Iron - metabolism iron overload lipid peroxidation Metabolic Diseases iron overload ferritinophagy ferroptosis metabolic diseases lipid peroxidation
ISSN:	1043-2760, 1879-3061, 1879-3061
Online Access:	Get full text
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Abstract	Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for targeting ferroptosis in the preservation of human health. Ferritinophagy, a selective form of autophagy, contributes to the initiation of ferroptosis through degradation of ferritin, which triggers labile iron overload (IO), lipid peroxidation, membrane damage, and cell death. In this review, we will delineate the role of ferritinophagy in ferroptosis, and its underlying regulatory mechanisms, to unveil the therapeutic value of ferritinophagy as a target in the combat of ferroptosis to manage metabolic diseases. Ferroptosis is a form of regulated cell death that is driven by iron overload and lipid peroxidation.Ferroptosis contributes to the onset or progression of various metabolic diseases.Ferritinophagy is a selective type of autophagy, which induces ferroptosis by degrading ferritin and inducing iron overload.Ferritinophagy inhibition may ameliorate ferroptosis and ease the management of metabolic diseases.
AbstractList	Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for targeting ferroptosis in the preservation of human health. Ferritinophagy, a selective form of autophagy, contributes to the initiation of ferroptosis through degradation of ferritin, which triggers labile iron overload (IO), lipid peroxidation, membrane damage, and cell death. In this review, we will delineate the role of ferritinophagy in ferroptosis, and its underlying regulatory mechanisms, to unveil the therapeutic value of ferritinophagy as a target in the combat of ferroptosis to manage metabolic diseases. Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for targeting ferroptosis in the preservation of human health. Ferritinophagy, a selective form of autophagy, contributes to the initiation of ferroptosis through degradation of ferritin, which triggers labile iron overload (IO), lipid peroxidation, membrane damage, and cell death. In this review, we will delineate the role of ferritinophagy in ferroptosis, and its underlying regulatory mechanisms, to unveil the therapeutic value of ferritinophagy as a target in the combat of ferroptosis to manage metabolic diseases.Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for targeting ferroptosis in the preservation of human health. Ferritinophagy, a selective form of autophagy, contributes to the initiation of ferroptosis through degradation of ferritin, which triggers labile iron overload (IO), lipid peroxidation, membrane damage, and cell death. In this review, we will delineate the role of ferritinophagy in ferroptosis, and its underlying regulatory mechanisms, to unveil the therapeutic value of ferritinophagy as a target in the combat of ferroptosis to manage metabolic diseases. Ferroptosis is a form of regulated cell death modality associated with disturbed iron-homeostasis and unrestricted lipid peroxidation. Ample evidence has depicted an essential role for ferroptosis as either the cause or consequence for human diseases, denoting the likely therapeutic promises for targeting ferroptosis in the preservation of human health. Ferritinophagy, a selective form of autophagy, contributes to the initiation of ferroptosis through degradation of ferritin, which triggers labile iron overload (IO), lipid peroxidation, membrane damage, and cell death. In this review, we will delineate the role of ferritinophagy in ferroptosis, and its underlying regulatory mechanisms, to unveil the therapeutic value of ferritinophagy as a target in the combat of ferroptosis to manage metabolic diseases. Ferroptosis is a form of regulated cell death that is driven by iron overload and lipid peroxidation.Ferroptosis contributes to the onset or progression of various metabolic diseases.Ferritinophagy is a selective type of autophagy, which induces ferroptosis by degrading ferritin and inducing iron overload.Ferritinophagy inhibition may ameliorate ferroptosis and ease the management of metabolic diseases.
Author	Aslkhodapasandhokmabad, Hamid Tang, Daolin Wang, Shuyi Richardson, Des R. Klionsky, Daniel J. Libby, Peter Zhou, Hao Ren, Jun Lip, Gregory Y.H. Ajoolabady, Amir Tuomilehto, Jaakko Penninger, Josef M. Kroemer, Guido
Author_xml	– sequence: 1 givenname: Amir surname: Ajoolabady fullname: Ajoolabady, Amir organization: Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA – sequence: 2 givenname: Hamid surname: Aslkhodapasandhokmabad fullname: Aslkhodapasandhokmabad, Hamid organization: University of Visayas, Gullas College of Medicine, Dionisio Jakosalem St, Cebu City, 6000, Cebu, Philippines – sequence: 3 givenname: Peter surname: Libby fullname: Libby, Peter organization: Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA – sequence: 4 givenname: Jaakko surname: Tuomilehto fullname: Tuomilehto, Jaakko organization: Public Health Promotion Unit, Finnish Institute for Health and Welfare, Helsinki, Finland – sequence: 5 givenname: Gregory Y.H. surname: Lip fullname: Lip, Gregory Y.H. organization: University of Liverpool Institute of Ageing and Chronic Disease, Liverpool Centre for Cardiovascular Science, Liverpool, UK – sequence: 6 givenname: Josef M. surname: Penninger fullname: Penninger, Josef M. organization: Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna Biocenter (VBC), Vienna, Austria – sequence: 7 givenname: Des R. surname: Richardson fullname: Richardson, Des R. organization: Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Medical Foundation Building (K25), University of Sydney, Sydney, New South Wales 2006, Australia – sequence: 8 givenname: Daolin surname: Tang fullname: Tang, Daolin organization: Department of Surgery, UT Southwestern Medical Center, Dallas, TX, 75390, USA – sequence: 9 givenname: Hao surname: Zhou fullname: Zhou, Hao organization: Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA – sequence: 10 givenname: Shuyi surname: Wang fullname: Wang, Shuyi email: shuyiwang23@outlook.com organization: Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA – sequence: 11 givenname: Daniel J. surname: Klionsky fullname: Klionsky, Daniel J. email: klionsky@umich.edu organization: Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 12 givenname: Guido surname: Kroemer fullname: Kroemer, Guido email: kroemer@orange.fr organization: Centre de Recherche des Cordeliers, Equipe Labellisée par la Ligue Contre le Cancer, Université de Paris, Sorbonne Université, Inserm U1138, Institut Universitaire de France, Paris, France – sequence: 13 givenname: Jun orcidid: 0000-0002-0275-0783 surname: Ren fullname: Ren, Jun email: jren_aldh2@outlook.com organization: Shanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai 200032, China
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34006412$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:$$DView record from Swedish Publication Index (Karolinska Institutet)
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SubjectTerms	Autophagy Endocrinology and Metabolism ferritinophagy Ferritins Ferroptosis Humans Iron - metabolism iron overload lipid peroxidation Metabolic Diseases
Title	Ferritinophagy and ferroptosis in the management of metabolic diseases
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