PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases
Carbohydrates and lipids are two components of the diet that provide the necessary energy to carry out various physiological processes to help maintain homeostasis in the body. However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as me...
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Veröffentlicht in: | International journal of molecular sciences 2021-08, Vol.22 (15), p.8298 |
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description | Carbohydrates and lipids are two components of the diet that provide the necessary energy to carry out various physiological processes to help maintain homeostasis in the body. However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as metabolic-associated fatty liver diseases (MAFLD), hepatitis B and C virus infections, alcoholic liver disease (ALD), and in more severe cases, hepatocelular carcinoma (HCC). On the other hand, PPARs are a family of ligand-dependent transcription factors with an important role in the regulation of metabolic processes to hepatic level as well as in other organs. After interaction with specific ligands, PPARs are translocated to the nucleus, undergoing structural changes to regulate gene transcription involved in lipid metabolism, adipogenesis, inflammation and metabolic homeostasis. This review aims to provide updated data about PPARs’ critical role in liver metabolic regulation, and their involvement triggering the genesis of several liver diseases. Information is provided about their molecular characteristics, cell signal pathways, and the main pharmacological therapies that modulate their function, currently engaged in the clinic scenario, or in pharmacological development. |
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However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as metabolic-associated fatty liver diseases (MAFLD), hepatitis B and C virus infections, alcoholic liver disease (ALD), and in more severe cases, hepatocelular carcinoma (HCC). On the other hand, PPARs are a family of ligand-dependent transcription factors with an important role in the regulation of metabolic processes to hepatic level as well as in other organs. After interaction with specific ligands, PPARs are translocated to the nucleus, undergoing structural changes to regulate gene transcription involved in lipid metabolism, adipogenesis, inflammation and metabolic homeostasis. This review aims to provide updated data about PPARs’ critical role in liver metabolic regulation, and their involvement triggering the genesis of several liver diseases. 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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as metabolic-associated fatty liver diseases (MAFLD), hepatitis B and C virus infections, alcoholic liver disease (ALD), and in more severe cases, hepatocelular carcinoma (HCC). On the other hand, PPARs are a family of ligand-dependent transcription factors with an important role in the regulation of metabolic processes to hepatic level as well as in other organs. After interaction with specific ligands, PPARs are translocated to the nucleus, undergoing structural changes to regulate gene transcription involved in lipid metabolism, adipogenesis, inflammation and metabolic homeostasis. This review aims to provide updated data about PPARs’ critical role in liver metabolic regulation, and their involvement triggering the genesis of several liver diseases. Information is provided about their molecular characteristics, cell signal pathways, and the main pharmacological therapies that modulate their function, currently engaged in the clinic scenario, or in pharmacological development.</description><subject>Adipogenesis</subject><subject>Biomolecules</subject><subject>Carbohydrates</subject><subject>Diet</subject><subject>Enzymes</subject><subject>Fatty acids</subject><subject>Fatty liver</subject><subject>Gastrointestinal surgery</subject><subject>Gene expression</subject><subject>hepatic damage</subject><subject>Hepatitis B</subject><subject>Hepatitis C</subject><subject>Homeostasis</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>metabolic alterations</subject><subject>Metabolism</subject><subject>nuclear factors</subject><subject>Organs</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>pharmacological targets</subject><subject>Pharmacology</subject><subject>Proteins</subject><subject>Review</subject><subject>Sensors</subject><subject>Signal transduction</subject><subject>Thyroid gland</subject><subject>Transcription factors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNpdkU1rFEEQhhtRTIze_AEDXjy4prv6cy5CSPwIrCTE9dzU9NRsepmdXrtnAv57Z7NBkpyqeOvhoahi7L3gn6Ws-WncbAuA0A5q94IdCwWw4NzYl4_6I_amlA3nIEHXr9mRVNIIbtQxu7i-PrspFZbqJ43YpD6G6hcNJeU5HNpqdUsZdzSNc77CvKaxVHGolvGOcnURC2Gh8pa96rAv9O6hnrDf376uzn8sllffL8_PlougtB4XggJJQk61qWtpOSpOthVdIywn6oySwgZHoEmooLuGAucI1mLousYEK0_Y5cHbJtz4XY5bzH99wujvg5TXHvO8aU8eJNlAoJSDoEJoGwPGOIFOIxgJMLu-HFy7qdlSG2gYM_ZPpE8nQ7z163TnnVTW1nvBxwdBTn8mKqPfxhKo73GgNBUPWtdKgrtHPzxDN2nKw3yqPeWc1Ibrmfp0oEJOpWTq_i8juN-_2j9-tfwHA6-aNw</recordid><startdate>20210801</startdate><enddate>20210801</enddate><creator>Monroy-Ramirez, Hugo Christian</creator><creator>Galicia-Moreno, Marina</creator><creator>Sandoval-Rodriguez, Ana</creator><creator>Meza-Rios, Alejandra</creator><creator>Santos, Arturo</creator><creator>Armendariz-Borunda, Juan</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1708-1495</orcidid><orcidid>https://orcid.org/0000-0002-1322-1684</orcidid><orcidid>https://orcid.org/0000-0002-7101-9943</orcidid></search><sort><creationdate>20210801</creationdate><title>PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases</title><author>Monroy-Ramirez, Hugo Christian ; 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subjects | Adipogenesis Biomolecules Carbohydrates Diet Enzymes Fatty acids Fatty liver Gastrointestinal surgery Gene expression hepatic damage Hepatitis B Hepatitis C Homeostasis Kinases Ligands Lipid metabolism Lipids Liver Liver diseases metabolic alterations Metabolism nuclear factors Organs Oxidation Oxidative stress pharmacological targets Pharmacology Proteins Review Sensors Signal transduction Thyroid gland Transcription factors |
title | PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases |
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