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Title:
GADD45A suppression contributes to cardiac remodeling by promoting inflammation, fibrosis and hypertrophy | Cellular and Molecular Life Sciences
Description:
The growth arrest and DNA damage inducible 45A (GADD45A) is a multifaceted protein associated with stress signaling and cellular injury. Aside its well-established tumor suppressor activity, recent studies point to additional roles for GADD45A, including the regulation of catabolic and anabolic pathways, or the prevention of inflammation, fibrosis, and oxidative stress in some tissues and organs. However, little is known about its function in cardiac disease. In this study, we aimed to evaluate the role of GADD45A in the heart by using mice with constitutive and systemic deletion of Gadd45a, and cardiac cells of human origin. Gadd45a suppression in knockout mice triggered cardiac fibrosis, inflammation, and apoptosis, and these changes correlated with an hyperactivation of the pro-inflammatory and pro-fibrotic transcription factors activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and signal transducer and activator of transcription 3 (STAT3). Deletion of Gadd45a also resulted in substantial cardiac hypertrophy, which negatively impacted cardiac morphology and function in knockout mice. Consistent with this, GADD45A overexpression in human AC16 cardiomyocytes partially prevented the inflammatory and fibrotic responses induced by tumor necrosis factor-α (TNF-α). Overall, data presented in this study highlight an important role for GADD45A in the heart, since it may prevent inflammation, fibrosis, and apoptosis, and, by this means, preserve cardiac function and performance. Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy and subsequent heart failure, these results suggest that promoting the activity of this protein might be a promising therapeutic strategy to slow down the progression of these deleterious diseases.
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Keywords {🔍}

gadda, pubmed, cardiac, mice, article, google, scholar, protein, heart, cas, expression, hypertrophy, fibrosis, fig, levels, cell, central, cells, apoptosis, glucose, stress, study, kinase, inflammation, mrna, activity, increased, data, gene, factor, human, transcription, muscle, reduced, metabolism, control, signaling, role, genes, function, atf, palomer, deletion, nfκb, activation, knockout, cardiomyocyte, samples, left, res,

Topics {✒️}

peroxisome proliferator-activated receptor c-jun n-terminal kinase c-jun nh2-terminal kinase impaired long-axis contraction atf4/tgf-beta1 signaling contributes downstream wnt/β-catenin pathway gadd45a-wnt/β-catenin pathway manuel vázquez-carrera 2d-guided m-mode echocardiography b-cell cll/lymphoma 2 amp-activated protein kinase article download pdf tnf-α-induced pro-inflammatory mitogen-activated protein kinases real-time rt-pcr protein-coupled receptor e1 western-blot analysis revealed β-myosin heavy chain tumor necrosis factor-α grants pid2021-122116ob-i00 high-fat diet tgf-beta/smad signaling α-myosin heavy chain mandarim-de-lacerda ca western-blot analyses revealed lgr4/hoxa9-dependent aml full pro-inflammatory profile cardiomyocyte cross-sectional areas left ventricular end-diastolic m-mlv reverse transcriptase improves fatty acid mtor/stat3 protein pathway cardiomyocyte cross-sectional area brenda valenzuela-alcaraz pressure overload situation serine/threonine kinase akt3 ebert sm dna damage inducible standard light-dark cycle high-fructose diets [79 nuclear factor kappab light-blue–stained area×100% phospho-stat3s727/total-stat3 fatty acid translocase tnf-α-induced increase tnf-α treatment boosted phospho-p38/total-p38 agarose gel electrophoresis holstein-rathlou nh transcription factor p53

Questions {❓}

Maron BA, Wang RS, Carnethon MR, Rowin EJ, Loscalzo J, Maron BJ, Maron MS (2022) What causes hypertrophic cardiomyopathy?
Palomer X, Pizarro-Delgado J, Vazquez-Carrera M (2018) Emerging actors in diabetic cardiomyopathy: heartbreaker biomarkers or therapeutic targets?
Pibarot P, Dumesnil JG (2010) Longitudinal myocardial shortening in aortic stenosis: ready for prime time after 30 years of research?

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         headline:GADD45A suppression contributes to cardiac remodeling by promoting inflammation, fibrosis and hypertrophy
         description:The growth arrest and DNA damage inducible 45A (GADD45A) is a multifaceted protein associated with stress signaling and cellular injury. Aside its well-established tumor suppressor activity, recent studies point to additional roles for GADD45A, including the regulation of catabolic and anabolic pathways, or the prevention of inflammation, fibrosis, and oxidative stress in some tissues and organs. However, little is known about its function in cardiac disease. In this study, we aimed to evaluate the role of GADD45A in the heart by using mice with constitutive and systemic deletion of Gadd45a, and cardiac cells of human origin. Gadd45a suppression in knockout mice triggered cardiac fibrosis, inflammation, and apoptosis, and these changes correlated with an hyperactivation of the pro-inflammatory and pro-fibrotic transcription factors activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and signal transducer and activator of transcription 3 (STAT3). Deletion of Gadd45a also resulted in substantial cardiac hypertrophy, which negatively impacted cardiac morphology and function in knockout mice. Consistent with this, GADD45A overexpression in human AC16 cardiomyocytes partially prevented the inflammatory and fibrotic responses induced by tumor necrosis factor-α (TNF-α). Overall, data presented in this study highlight an important role for GADD45A in the heart, since it may prevent inflammation, fibrosis, and apoptosis, and, by this means, preserve cardiac function and performance. Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy and subsequent heart failure, these results suggest that promoting the activity of this protein might be a promising therapeutic strategy to slow down the progression of these deleterious diseases.
         datePublished:2025-04-30T00:00:00Z
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            Cell Biology
            Biomedicine
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      headline:GADD45A suppression contributes to cardiac remodeling by promoting inflammation, fibrosis and hypertrophy
      description:The growth arrest and DNA damage inducible 45A (GADD45A) is a multifaceted protein associated with stress signaling and cellular injury. Aside its well-established tumor suppressor activity, recent studies point to additional roles for GADD45A, including the regulation of catabolic and anabolic pathways, or the prevention of inflammation, fibrosis, and oxidative stress in some tissues and organs. However, little is known about its function in cardiac disease. In this study, we aimed to evaluate the role of GADD45A in the heart by using mice with constitutive and systemic deletion of Gadd45a, and cardiac cells of human origin. Gadd45a suppression in knockout mice triggered cardiac fibrosis, inflammation, and apoptosis, and these changes correlated with an hyperactivation of the pro-inflammatory and pro-fibrotic transcription factors activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and signal transducer and activator of transcription 3 (STAT3). Deletion of Gadd45a also resulted in substantial cardiac hypertrophy, which negatively impacted cardiac morphology and function in knockout mice. Consistent with this, GADD45A overexpression in human AC16 cardiomyocytes partially prevented the inflammatory and fibrotic responses induced by tumor necrosis factor-α (TNF-α). Overall, data presented in this study highlight an important role for GADD45A in the heart, since it may prevent inflammation, fibrosis, and apoptosis, and, by this means, preserve cardiac function and performance. Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy and subsequent heart failure, these results suggest that promoting the activity of this protein might be a promising therapeutic strategy to slow down the progression of these deleterious diseases.
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      dateModified:2025-04-30T00:00:00Z
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      pageEnd:22
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      sameAs:https://doi.org/10.1007/s00018-025-05704-x
      keywords:
         Apoptosis
         Cardiac hypertrophy
         GADD45A
         Inflammation and fibrosis
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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