Modulatory effects of CNNM4 on protein-L-isoaspartylO-methyltransferase repair function during alcohol-induced hepatic damage

Background and Aims: Alcohol-associated liver disease (ALD) is a,leading cause of liver-related mortality worldwide, with limited treatment,options beyond abstinence and liver transplantation. Chronic alcohol,consumption has been linked to magnesium (Mg2+) deficiency, which can,influence liver disea...

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Detalles Bibliográficos
Autores: González Recio, Irene, Goikoetxea Usandizaga, Naroa, Rejano Gordillo, Claudia M., Conter, Carolina, Rodríguez Agudo, Rubén, Serrano Maciá, Marina, Díaz Moreno, Irene, Díaz Quintana, Antonio Jesús, Martínez Chantar, María Luz
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/174220
Acceso en línea:https://hdl.handle.net/11441/174220
https://doi.org/10.1097/HEP.0000000000001156
Access Level:acceso abierto
Palabra clave:Alcohol
ALD
Hepatotoxicity
Magnesium
Descripción
Sumario:Background and Aims: Alcohol-associated liver disease (ALD) is a,leading cause of liver-related mortality worldwide, with limited treatment,options beyond abstinence and liver transplantation. Chronic alcohol,consumption has been linked to magnesium (Mg2+) deficiency, which can,influence liver disease progression. The mechanisms underlying Mg2+,homeostasis dysregulation in ALD remain elusive. This study aimed to,investigate the role of the Mg2+ transporter Cyclin M4 (CNNM4) in ALD by,analyzing its expression patterns in patients with ALD and preclinical,animal models.,Approach and Results: In this study, CNNM4 is upregulated in the liver of,both patients with ALD and animal models. CNNM4 overexpression triggers Mg2+ homeostasis dysregulation, linked to ALD progression. We,propose a novel therapeutic approach for ALD treatment using N-acetylgalactosamine silencing RNA technology to specifically modulate,Cnnm4 expression in the liver, improving mitochondrial function and alleviating endoplasmic reticulum stress. Notably, silencing Cnnm4 restores,protein isoaspartyl methyltransferase (PCMT1) activity, essential for,repairing ethanol-induced protein damage. Enhancing mitochondrial,activity through Cnnm4-dependent mechanisms increases S-adenosylmethionine levels, crucial for PCMT1 function, highlighting the interconnected roles of mitochondrial health and protein homeostasis in ALD,treatment.,Conclusions: These findings shed light on the dysregulation of Mg2+,homeostasis in ALD, providing a promising therapeutic approach targeting,CNNM4. N-acetylgalactosamine siCnnm4 therapy boosts the repair processes of ethanol-damaged proteins through the upregulation of PCMT1,activity.