The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury

Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP cause...

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Published inNature communications Vol. 8; no. 1; pp. 2068 - 11
Main Authors Barbier-Torres, Lucía, Iruzubieta, Paula, Fernández-Ramos, David, Delgado, Teresa C., Taibo, Daniel, Guitiérrez-de-Juan, Virginia, Varela-Rey, Marta, Azkargorta, Mikel, Navasa, Nicolas, Fernández-Tussy, Pablo, Zubiete-Franco, Imanol, Simon, Jorge, Lopitz-Otsoa, Fernando, Lachiondo-Ortega, Sofia, Crespo, Javier, Masson, Steven, McCain, Misti Vanette, Villa, Erica, Reeves, Helen, Elortza, Felix, Lucena, Maria Isabel, Hernández-Alvarez, Maria Isabel, Zorzano, Antonio, Andrade, Raúl J., Lu, Shelly C., Mato, José M., Anguita, Juan, Rincón, Mercedes, Martínez-Chantar, María Luz
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 12.12.2017
Nature Publishing Group
Nature Portfolio
Subjects
631/80/642/333
692/4020/4021/1607/2749
Acetaminophen
Acetaminophen - toxicity
Acetylcysteine
Adolescent
Adult
Analgesics
Animals
Biocompatibility
Chemical and Drug Induced Liver Injury - drug therapy
Chemical and Drug Induced Liver Injury - etiology
Chemical and Drug Induced Liver Injury - pathology
Disease Models, Animal
Down-regulation
Drug Overdose - complications
Drug Overdose - etiology
Electron Transport Complex I - metabolism
Female
Fever
Gene Knockout Techniques
Hepatocytes
HSP40 Heat-Shock Proteins - antagonists & inhibitors
HSP40 Heat-Shock Proteins - metabolism
Humanities and Social Sciences
Humans
Injury prevention
Liver
Liver - cytology
Liver - pathology
Liver diseases
Male
Mice
Mice, Inbred C57BL
Middle Aged
Mitochondria
Mitochondria, Liver - metabolism
Mitochondrial Proteins - antagonists & inhibitors
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Molecular Chaperones - antagonists & inhibitors
Molecular Chaperones - genetics
Molecular Chaperones - metabolism
multidisciplinary
Overdose
Pain
Primary Cell Culture
RNA, Small Interfering - metabolism
Rotenone - pharmacology
Rotenone - therapeutic use
Science
Science (multidisciplinary)
Toxicity
Uncoupling Agents - pharmacology
Uncoupling Agents - therapeutic use
Young Adult
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-017-01970-x

Cover

Abstract Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N -acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen. Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et al. show that targeting MCJ, a mitochondrial negative regulator, even 24 h after the overdose protects liver from acetaminophen-induced damage.
AbstractList Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.
Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N -acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.
Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.
Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N -acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen. Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et al. show that targeting MCJ, a mitochondrial negative regulator, even 24 h after the overdose protects liver from acetaminophen-induced damage.
Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et al. show that targeting MCJ, a mitochondrial negative regulator, even 24 h after the overdose protects liver from acetaminophen-induced damage.
Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen. Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et al. show that targeting MCJ, a mitochondrial negative regulator, even 24 h after the overdose protects liver from acetaminophen-induced damage.
ArticleNumber 2068
Author Barbier-Torres, Lucía
Zubiete-Franco, Imanol
Anguita, Juan
Martínez-Chantar, María Luz
Fernández-Tussy, Pablo
Simon, Jorge
Elortza, Felix
Taibo, Daniel
Mato, José M.
Fernández-Ramos, David
Masson, Steven
McCain, Misti Vanette
Iruzubieta, Paula
Lu, Shelly C.
Zorzano, Antonio
Andrade, Raúl J.
Delgado, Teresa C.
Varela-Rey, Marta
Azkargorta, Mikel
Rincón, Mercedes
Villa, Erica
Reeves, Helen
Hernández-Alvarez, Maria Isabel
Crespo, Javier
Lachiondo-Ortega, Sofia
Navasa, Nicolas
Lopitz-Otsoa, Fernando
Lucena, Maria Isabel
Guitiérrez-de-Juan, Virginia
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/29233977$$D View this record in MEDLINE/PubMed
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Snippet Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second...
Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et...
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StartPage 2068
SubjectTerms 631/80/642/333
692/4020/4021/1607/2749
Acetaminophen
Acetaminophen - toxicity
Acetylcysteine
Adolescent
Adult
Analgesics
Animals
Biocompatibility
Chemical and Drug Induced Liver Injury - drug therapy
Chemical and Drug Induced Liver Injury - etiology
Chemical and Drug Induced Liver Injury - pathology
Disease Models, Animal
Down-regulation
Drug Overdose - complications
Drug Overdose - etiology
Electron Transport Complex I - metabolism
Female
Fever
Gene Knockout Techniques
Hepatocytes
HSP40 Heat-Shock Proteins - antagonists & inhibitors
HSP40 Heat-Shock Proteins - metabolism
Humanities and Social Sciences
Humans
Injury prevention
Liver
Liver - cytology
Liver - pathology
Liver diseases
Male
Mice
Mice, Inbred C57BL
Middle Aged
Mitochondria
Mitochondria, Liver - metabolism
Mitochondrial Proteins - antagonists & inhibitors
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Molecular Chaperones - antagonists & inhibitors
Molecular Chaperones - genetics
Molecular Chaperones - metabolism
multidisciplinary
Overdose
Pain
Primary Cell Culture
RNA, Small Interfering - metabolism
Rotenone - pharmacology
Rotenone - therapeutic use
Science
Science (multidisciplinary)
Toxicity
Uncoupling Agents - pharmacology
Uncoupling Agents - therapeutic use
Young Adult
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Title The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury
URI https://link.springer.com/article/10.1038/s41467-017-01970-x
https://www.ncbi.nlm.nih.gov/pubmed/29233977
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https://pubmed.ncbi.nlm.nih.gov/PMC5727217
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