Amelioration of nephrotoxicity by targeting ferroptosis: role of NCOA4, IREB2, and SLC7a11 signaling

Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated....

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Published inBrazilian journal of medical and biological research Vol. 57; p. e13116
Main Authors Sharawy, N, Aboulhoda, B E, Khalifa, M M, Morcos, G N, Morsy, S A A G, Alghamdi, M A, Khalifa, I M, Abd Algaleel, W A
Format Journal Article
LanguageEnglish
Published Brazil Associação Brasileira de Divulgação Científica 01.01.2024
Subjects
Amino Acid Transport System y+ - metabolism
Animals
Antineoplastic Agents
BIOLOGY
Cisplatin
Cisplatin - toxicity
Deferiprone
Deferiprone - pharmacology
Ferritinophagy
Ferritins - metabolism
Ferroptosis
Ferroptosis - drug effects
Immunohistochemistry
Iron
Iron - metabolism
Kidney
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Kidney Diseases - chemically induced
Kidney Diseases - metabolism
Lipid Peroxidation - drug effects
Male
MEDICINE, RESEARCH & EXPERIMENTAL
Nuclear Receptor Coactivators - metabolism
Rats
Rats, Sprague-Dawley
Signal Transduction - drug effects
Ferroptosis
Ferritinophagy
Iron
Deferiprone
Kidney
Cisplatin
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Abstract Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated. In this study, we aimed to investigate the involvement of nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor that mediates ferroptosis and autophagic degradation of ferritin in nephrotoxicity. Adult male Sprague-Dawley rats were randomly-assigned to four groups: control group, cisplatin (Cis)-treated group, deferiprone (DEF)-treated group, and Cis+DEF co-treated group. Serum, urine, and kidneys were isolated to perform biochemical, morphometric, and immunohistochemical analysis. Iron accumulation was found to predispose to ferroptotic damage of the renal tubular cells. Treatment with deferiprone highlights the role of ferroptosis in nephrotoxicity. Upregulation of NCOA4 in parallel with low ferritin level in renal tissue seems to participate in iron-induced ferroptosis. This study indicated that ferroptosis may participate in cisplatin-induced tubular cell death and nephrotoxicity through iron-mediated lipid peroxidation. Iron dyshomeostasis could be attributed to NCOA4-mediated ferritin degradation.
AbstractList Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated. In this study, we aimed to investigate the involvement of nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor that mediates ferroptosis and autophagic degradation of ferritin in nephrotoxicity. Adult male Sprague-Dawley rats were randomly-assigned to four groups: control group, cisplatin (Cis)-treated group, deferiprone (DEF)-treated group, and Cis+DEF co-treated group. Serum, urine, and kidneys were isolated to perform biochemical, morphometric, and immunohistochemical analysis. Iron accumulation was found to predispose to ferroptotic damage of the renal tubular cells. Treatment with deferiprone highlights the role of ferroptosis in nephrotoxicity. Upregulation of NCOA4 in parallel with low ferritin level in renal tissue seems to participate in iron-induced ferroptosis. This study indicated that ferroptosis may participate in cisplatin-induced tubular cell death and nephrotoxicity through iron-mediated lipid peroxidation. Iron dyshomeostasis could be attributed to NCOA4-mediated ferritin degradation.Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated. In this study, we aimed to investigate the involvement of nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor that mediates ferroptosis and autophagic degradation of ferritin in nephrotoxicity. Adult male Sprague-Dawley rats were randomly-assigned to four groups: control group, cisplatin (Cis)-treated group, deferiprone (DEF)-treated group, and Cis+DEF co-treated group. Serum, urine, and kidneys were isolated to perform biochemical, morphometric, and immunohistochemical analysis. Iron accumulation was found to predispose to ferroptotic damage of the renal tubular cells. Treatment with deferiprone highlights the role of ferroptosis in nephrotoxicity. Upregulation of NCOA4 in parallel with low ferritin level in renal tissue seems to participate in iron-induced ferroptosis. This study indicated that ferroptosis may participate in cisplatin-induced tubular cell death and nephrotoxicity through iron-mediated lipid peroxidation. Iron dyshomeostasis could be attributed to NCOA4-mediated ferritin degradation.
Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated. In this study, we aimed to investigate the involvement of nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor that mediates ferroptosis and autophagic degradation of ferritin in nephrotoxicity. Adult male Sprague-Dawley rats were randomly-assigned to four groups: control group, cisplatin (Cis)-treated group, deferiprone (DEF)-treated group, and Cis+DEF co-treated group. Serum, urine, and kidneys were isolated to perform biochemical, morphometric, and immunohistochemical analysis. Iron accumulation was found to predispose to ferroptotic damage of the renal tubular cells. Treatment with deferiprone highlights the role of ferroptosis in nephrotoxicity. Upregulation of NCOA4 in parallel with low ferritin level in renal tissue seems to participate in iron-induced ferroptosis. This study indicated that ferroptosis may participate in cisplatin-induced tubular cell death and nephrotoxicity through iron-mediated lipid peroxidation. Iron dyshomeostasis could be attributed to NCOA4-mediated ferritin degradation.
Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is mediated by phospholipid peroxidation. The molecular mechanisms that disrupt iron homeostasis and lead to ferroptosis are yet to be elucidated. In this study, we aimed to investigate the involvement of nuclear receptor coactivator 4 ( NCOA4 ), a selective cargo receptor that mediates ferroptosis and autophagic degradation of ferritin in nephrotoxicity. Adult male Sprague-Dawley rats were randomly-assigned to four groups: control group, cisplatin (Cis)-treated group, deferiprone (DEF)-treated group, and Cis+DEF co-treated group. Serum, urine, and kidneys were isolated to perform biochemical, morphometric, and immunohistochemical analysis. Iron accumulation was found to predispose to ferroptotic damage of the renal tubular cells. Treatment with deferiprone highlights the role of ferroptosis in nephrotoxicity. Upregulation of NCOA4 in parallel with low ferritin level in renal tissue seems to participate in iron-induced ferroptosis. This study indicated that ferroptosis may participate in cisplatin-induced tubular cell death and nephrotoxicity through iron-mediated lipid peroxidation. Iron dyshomeostasis could be attributed to NCOA4 -mediated ferritin degradation.
Author Sharawy, N
Morsy, S A A G
Khalifa, M M
Abd Algaleel, W A
Morcos, G N
Khalifa, I M
Aboulhoda, B E
Alghamdi, M A
AuthorAffiliation King Salman International University
Fakeeh College for Medical Sciences
Ain Shams University
Alexandria University
College of Medicine, King Khalid University
King Khalid University
Galala University
King Saud University
Cairo University
AuthorAffiliation_xml – name: Galala University
– name: Cairo University
– name: Fakeeh College for Medical Sciences
– name: King Saud University
– name: King Salman International University
– name: King Khalid University
– name: Alexandria University
– name: College of Medicine, King Khalid University
– name: Ain Shams University
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  orcidid: 0000-0002-3311-8879
  surname: Sharawy
  fullname: Sharawy, N
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Keywords Ferroptosis
Ferritinophagy
Iron
Deferiprone
Kidney
Cisplatin
Language English
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SSID ssj0025041
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Snippet Nephrotoxicity is a common complication that limits the clinical utility of cisplatin. Ferroptosis is an iron-dependent necrotic cell death program that is...
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SubjectTerms Amino Acid Transport System y+ - metabolism
Animals
Antineoplastic Agents
BIOLOGY
Cisplatin
Cisplatin - toxicity
Deferiprone
Deferiprone - pharmacology
Ferritinophagy
Ferritins - metabolism
Ferroptosis
Ferroptosis - drug effects
Immunohistochemistry
Iron
Iron - metabolism
Kidney
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Kidney Diseases - chemically induced
Kidney Diseases - metabolism
Lipid Peroxidation - drug effects
Male
MEDICINE, RESEARCH & EXPERIMENTAL
Nuclear Receptor Coactivators - metabolism
Rats
Rats, Sprague-Dawley
Signal Transduction - drug effects
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Title Amelioration of nephrotoxicity by targeting ferroptosis: role of NCOA4, IREB2, and SLC7a11 signaling
URI https://www.ncbi.nlm.nih.gov/pubmed/39383377
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Volume 57
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