Molecular Basis of Cardiomyopathies in Type 2 Diabetes
Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functi...
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| Veröffentlicht in: | International journal of molecular sciences 2024-08, Vol.25 (15), p.8280 |
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| creator | Giardinelli, Silvia Meliota, Giovanni Mentino, Donatella D'Amato, Gabriele Faienza, Maria Felicia |
| description | Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways. |
| doi_str_mv | 10.3390/ijms25158280 |
| format | Article |
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It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25158280</identifier><identifier>PMID: 39125850</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antigens ; Apoptosis ; Apoptosis - genetics ; Autophagy ; B cells ; Body fat ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular disease ; Cytokines ; Development and progression ; Diabetes ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetic Cardiomyopathies - etiology ; Diabetic Cardiomyopathies - genetics ; Diabetic Cardiomyopathies - metabolism ; Diabetic Cardiomyopathies - pathology ; Epigenesis, Genetic ; Epigenetic inheritance ; Glucose ; Heart enlargement ; Heart failure ; Humans ; Hyperglycemia ; Inflammation ; Insulin Resistance ; Kinases ; Lipids ; Metabolism ; Mitochondria ; Mortality ; Musculoskeletal system ; Myocardium - metabolism ; Myocardium - pathology ; Oxidation ; Oxidative Stress ; Phosphorylation ; Physiological aspects ; Proteins ; Tumor necrosis factor-TNF ; Type 2 diabetes</subject><ispartof>International journal of molecular sciences, 2024-08, Vol.25 (15), p.8280</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. 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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Meliota, Giovanni ; Mentino, Donatella ; D'Amato, Gabriele ; Faienza, Maria Felicia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-b25dbb06102a29e384925746e80fbb0d4c92c3b978eebc2419aa30965068fe73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Autophagy</topic><topic>B cells</topic><topic>Body fat</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular disease</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetic Cardiomyopathies - etiology</topic><topic>Diabetic Cardiomyopathies - genetics</topic><topic>Diabetic Cardiomyopathies - metabolism</topic><topic>Diabetic Cardiomyopathies - pathology</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetic inheritance</topic><topic>Glucose</topic><topic>Heart enlargement</topic><topic>Heart failure</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Insulin Resistance</topic><topic>Kinases</topic><topic>Lipids</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mortality</topic><topic>Musculoskeletal system</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Oxidation</topic><topic>Oxidative Stress</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Tumor necrosis factor-TNF</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Giardinelli, Silvia</creatorcontrib><creatorcontrib>Meliota, Giovanni</creatorcontrib><creatorcontrib>Mentino, Donatella</creatorcontrib><creatorcontrib>D'Amato, Gabriele</creatorcontrib><creatorcontrib>Faienza, Maria Felicia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Giardinelli, Silvia</au><au>Meliota, Giovanni</au><au>Mentino, Donatella</au><au>D'Amato, Gabriele</au><au>Faienza, Maria Felicia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular Basis of Cardiomyopathies in Type 2 Diabetes</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-08-01</date><risdate>2024</risdate><volume>25</volume><issue>15</issue><spage>8280</spage><pages>8280-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39125850</pmid><doi>10.3390/ijms25158280</doi><orcidid>https://orcid.org/0000-0002-9924-4915</orcidid><orcidid>https://orcid.org/0000-0002-1899-8337</orcidid><orcidid>https://orcid.org/0000-0002-0680-5251</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens Apoptosis Apoptosis - genetics Autophagy B cells Body fat Cardiomyocytes Cardiomyopathy Cardiovascular disease Cytokines Development and progression Diabetes Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetic Cardiomyopathies - etiology Diabetic Cardiomyopathies - genetics Diabetic Cardiomyopathies - metabolism Diabetic Cardiomyopathies - pathology Epigenesis, Genetic Epigenetic inheritance Glucose Heart enlargement Heart failure Humans Hyperglycemia Inflammation Insulin Resistance Kinases Lipids Metabolism Mitochondria Mortality Musculoskeletal system Myocardium - metabolism Myocardium - pathology Oxidation Oxidative Stress Phosphorylation Physiological aspects Proteins Tumor necrosis factor-TNF Type 2 diabetes |
| title | Molecular Basis of Cardiomyopathies in Type 2 Diabetes |
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