Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function

Background & aims: Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which is essential for autophagy. Whether ATG3 plays a role in lipid metabolism or contributes to non-alcoholic fatty liver disease (NAFLD) remains unknown. Methods: By per...

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Autores: da Silva Lima, Natália, Fondevila, Marcos F., Novoa Pardo, Eva Maria, Buqué, Xabier, Mercado-Gómez, Maria, Gallet, Sarah, González-Rellan, Maria J., Fernandez, Uxia, Loyens, Anne, García-Vence, Maria, Chantada-Vázquez, Maria Del Pilar, Bravo, Susana, Marañon, Patricia, Senra, Ana, Escudero, Adriana, Leiva, Magdalena, Guallar, Diana, Fidalgo, Miguel, Gomes, Pedro, Claret i Carles, Marc, Sabio, Guadalupe, Varela Rey, Marta, Delgado, Teresa C., Montero-Vallejo, Rocio, Ampuero, Javier, López, Miguel, Diéguez, Carlos, Herrero Rodríguez, Laura, Serra i Cucurull, Dolors, Schwaninger, Markus, Prevot, Vincent, Gallego Durán, Rocío, Romero Gómez, Manuel 1967-, Iruzubieta, Paula, Crespo, Javier, Martínez Chantar, Maria Luz, García Monzón, Carmelo, González Rodríguez, Águeda, Aspichueta, Patricia, Nogueiras, Rubén
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2021
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/184087
Acceso en línea:https://hdl.handle.net/2445/184087
Access Level:acceso abierto
Palabra clave:Metabolisme dels lípids
Mitocondris
Lipid metabolism
Mitochondria
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spelling Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial functionda Silva Lima, NatáliaFondevila, Marcos F.Novoa Pardo, Eva MariaBuqué, XabierMercado-Gómez, MariaGallet, SarahGonzález-Rellan, Maria J.Fernandez, UxiaLoyens, AnneGarcía-Vence, MariaChantada-Vázquez, Maria Del PilarBravo, SusanaMarañon, PatriciaSenra, AnaEscudero, AdrianaLeiva, MagdalenaGuallar, DianaFidalgo, MiguelGomes, PedroClaret i Carles, MarcSabio, GuadalupeVarela Rey, MartaDelgado, Teresa C.Montero-Vallejo, RocioAmpuero, JavierLópez, MiguelDiéguez, CarlosHerrero Rodríguez, LauraSerra i Cucurull, DolorsSchwaninger, MarkusPrevot, VincentGallego Durán, RocíoRomero Gómez, Manuel 1967-Iruzubieta, PaulaCrespo, JavierMartínez Chantar, Maria LuzGarcía Monzón, CarmeloGonzález Rodríguez, ÁguedaAspichueta, PatriciaNogueiras, RubénMetabolisme dels lípidsMitocondrisLipid metabolismMitochondriaBackground & aims: Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which is essential for autophagy. Whether ATG3 plays a role in lipid metabolism or contributes to non-alcoholic fatty liver disease (NAFLD) remains unknown. Methods: By performing proteomic analysis on livers from mice with genetic manipulation of hepatic p63, a regulator of fatty acid metabolism, we identified ATG3 as a new target downstream of p63. ATG3 was evaluated in liver samples from patients with NAFLD. Further, genetic manipulation of ATG3 was performed in human hepatocyte cell lines, primary hepatocytes and in the livers of mice. Results: ATG3 expression is induced in the liver of animal models and patients with NAFLD (both steatosis and non-alcoholic steatohepatitis) compared with those without liver disease. Moreover, genetic knockdown of ATG3 in mice and human hepatocytes ameliorates p63- and diet-induced steatosis, while its overexpression increases the lipid load in hepatocytes. The inhibition of hepatic ATG3 improves fatty acid metabolism by reducing c-Jun N-terminal protein kinase 1 (JNK1), which increases sirtuin 1 (SIRT1), carnitine palmitoyltransferase 1a (CPT1a), and mitochondrial function. Hepatic knockdown of SIRT1 and CPT1a blunts the effects of ATG3 on mitochondrial activity. Unexpectedly, these effects are independent of an autophagic action. Conclusions: Collectively, these findings indicate that ATG3 is a novel protein implicated in the development of steatosis. Lay summary: We show that autophagy-related gene 3 (ATG3) contributes to the progression of non-alcoholic fatty liver disease in humans and mice. Hepatic knockdown of ATG3 ameliorates the development of NAFLD by stimulating mitochondrial function. Thus, ATG3 is an important factor implicated in steatosis. Keywords: ATG3; NAFLD; NASH; lipid metabolism; mitochondria; sirtuin 1.Elsevier2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/2445/184087Articles publicats en revistes (Bioquímica i Fisiologia)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésVersió postprint del document publicat a: https://doi.org/10.1016/j.jhep.2021.09.008Journal of Hepatology, 2021, vol. 76, p. 11-14https://doi.org/10.1016/j.jhep.2021.09.008cc-by-nc-nd (c) Elsevier, 2021https://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1840872026-05-27T06:46:51Z
dc.title.none.fl_str_mv Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
title Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
spellingShingle Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
da Silva Lima, Natália
Metabolisme dels lípids
Mitocondris
Lipid metabolism
Mitochondria
title_short Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
title_full Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
title_fullStr Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
title_full_unstemmed Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
title_sort Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function
dc.creator.none.fl_str_mv da Silva Lima, Natália
Fondevila, Marcos F.
Novoa Pardo, Eva Maria
Buqué, Xabier
Mercado-Gómez, Maria
Gallet, Sarah
González-Rellan, Maria J.
Fernandez, Uxia
Loyens, Anne
García-Vence, Maria
Chantada-Vázquez, Maria Del Pilar
Bravo, Susana
Marañon, Patricia
Senra, Ana
Escudero, Adriana
Leiva, Magdalena
Guallar, Diana
Fidalgo, Miguel
Gomes, Pedro
Claret i Carles, Marc
Sabio, Guadalupe
Varela Rey, Marta
Delgado, Teresa C.
Montero-Vallejo, Rocio
Ampuero, Javier
López, Miguel
Diéguez, Carlos
Herrero Rodríguez, Laura
Serra i Cucurull, Dolors
Schwaninger, Markus
Prevot, Vincent
Gallego Durán, Rocío
Romero Gómez, Manuel 1967-
Iruzubieta, Paula
Crespo, Javier
Martínez Chantar, Maria Luz
García Monzón, Carmelo
González Rodríguez, Águeda
Aspichueta, Patricia
Nogueiras, Rubén
author da Silva Lima, Natália
author_facet da Silva Lima, Natália
Fondevila, Marcos F.
Novoa Pardo, Eva Maria
Buqué, Xabier
Mercado-Gómez, Maria
Gallet, Sarah
González-Rellan, Maria J.
Fernandez, Uxia
Loyens, Anne
García-Vence, Maria
Chantada-Vázquez, Maria Del Pilar
Bravo, Susana
Marañon, Patricia
Senra, Ana
Escudero, Adriana
Leiva, Magdalena
Guallar, Diana
Fidalgo, Miguel
Gomes, Pedro
Claret i Carles, Marc
Sabio, Guadalupe
Varela Rey, Marta
Delgado, Teresa C.
Montero-Vallejo, Rocio
Ampuero, Javier
López, Miguel
Diéguez, Carlos
Herrero Rodríguez, Laura
Serra i Cucurull, Dolors
Schwaninger, Markus
Prevot, Vincent
Gallego Durán, Rocío
Romero Gómez, Manuel 1967-
Iruzubieta, Paula
Crespo, Javier
Martínez Chantar, Maria Luz
García Monzón, Carmelo
González Rodríguez, Águeda
Aspichueta, Patricia
Nogueiras, Rubén
author_role author
author2 Fondevila, Marcos F.
Novoa Pardo, Eva Maria
Buqué, Xabier
Mercado-Gómez, Maria
Gallet, Sarah
González-Rellan, Maria J.
Fernandez, Uxia
Loyens, Anne
García-Vence, Maria
Chantada-Vázquez, Maria Del Pilar
Bravo, Susana
Marañon, Patricia
Senra, Ana
Escudero, Adriana
Leiva, Magdalena
Guallar, Diana
Fidalgo, Miguel
Gomes, Pedro
Claret i Carles, Marc
Sabio, Guadalupe
Varela Rey, Marta
Delgado, Teresa C.
Montero-Vallejo, Rocio
Ampuero, Javier
López, Miguel
Diéguez, Carlos
Herrero Rodríguez, Laura
Serra i Cucurull, Dolors
Schwaninger, Markus
Prevot, Vincent
Gallego Durán, Rocío
Romero Gómez, Manuel 1967-
Iruzubieta, Paula
Crespo, Javier
Martínez Chantar, Maria Luz
García Monzón, Carmelo
González Rodríguez, Águeda
Aspichueta, Patricia
Nogueiras, Rubén
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Metabolisme dels lípids
Mitocondris
Lipid metabolism
Mitochondria
topic Metabolisme dels lípids
Mitocondris
Lipid metabolism
Mitochondria
description Background & aims: Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which is essential for autophagy. Whether ATG3 plays a role in lipid metabolism or contributes to non-alcoholic fatty liver disease (NAFLD) remains unknown. Methods: By performing proteomic analysis on livers from mice with genetic manipulation of hepatic p63, a regulator of fatty acid metabolism, we identified ATG3 as a new target downstream of p63. ATG3 was evaluated in liver samples from patients with NAFLD. Further, genetic manipulation of ATG3 was performed in human hepatocyte cell lines, primary hepatocytes and in the livers of mice. Results: ATG3 expression is induced in the liver of animal models and patients with NAFLD (both steatosis and non-alcoholic steatohepatitis) compared with those without liver disease. Moreover, genetic knockdown of ATG3 in mice and human hepatocytes ameliorates p63- and diet-induced steatosis, while its overexpression increases the lipid load in hepatocytes. The inhibition of hepatic ATG3 improves fatty acid metabolism by reducing c-Jun N-terminal protein kinase 1 (JNK1), which increases sirtuin 1 (SIRT1), carnitine palmitoyltransferase 1a (CPT1a), and mitochondrial function. Hepatic knockdown of SIRT1 and CPT1a blunts the effects of ATG3 on mitochondrial activity. Unexpectedly, these effects are independent of an autophagic action. Conclusions: Collectively, these findings indicate that ATG3 is a novel protein implicated in the development of steatosis. Lay summary: We show that autophagy-related gene 3 (ATG3) contributes to the progression of non-alcoholic fatty liver disease in humans and mice. Hepatic knockdown of ATG3 ameliorates the development of NAFLD by stimulating mitochondrial function. Thus, ATG3 is an important factor implicated in steatosis. Keywords: ATG3; NAFLD; NASH; lipid metabolism; mitochondria; sirtuin 1.
publishDate 2021
dc.date.none.fl_str_mv 2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/184087
url https://hdl.handle.net/2445/184087
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: https://doi.org/10.1016/j.jhep.2021.09.008
Journal of Hepatology, 2021, vol. 76, p. 11-14
https://doi.org/10.1016/j.jhep.2021.09.008
dc.rights.none.fl_str_mv cc-by-nc-nd (c) Elsevier, 2021
https://creativecommons.org/licenses/by-nc-nd/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by-nc-nd (c) Elsevier, 2021
https://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv Articles publicats en revistes (Bioquímica i Fisiologia)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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