ArticleInternational journal of molecular sciences2019
Deletion of Osteopontin Enhances β₂-Adrenergic Receptor-Dependent Anti-Fibrotic Signaling in Cardiomyocytes.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Epac1 Inhibits Orbital Fibroblast Activation to Ameliorate Thyroid-Associated Orbitopathy-Like Features Through the JAK/STAT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
- Identification of Necroptosis and Immune Infiltration in Heart Failure Through Bioinformatics Analysis.Journal of inflammation research · 2025Article
- Expression of Osteopontin and Gremlin 1 Proteins in Cardiomyocytes in Ischemic Heart Failure.International journal of molecular sciences · 2024Article
- Cyclic Adenosine Monophosphate in Cardiac and Sympathoadrenal GLP-1 Receptor Signaling: Focus on Anti-Inflammatory Effects.Pharmaceutics · 2024Review
- An Overview of the Mechanism behind Excessive Volume of Pericardial Fat in Heart Failure.Journal of obesity & metabolic syndrome · 2023Review
- ADRB2 inhibition combined with antioxidant treatment alleviates lung fibrosis by attenuating TGFβ/SMAD signaling in lung fibroblasts.Cell death discovery · 2023Article
- Differential Role of Aldosterone and Transforming Growth Factor Beta-1 in Cardiac Remodeling.International journal of molecular sciences · 2023Article
- Editorial to theInternational journal of molecular sciences · 2023Article
- Experimental study on the effect of chlorhexidine gluconate (CG)-induced atrial fibrillation on renal water and sodium metabolism.Scientific reports · 2023Article
- Autonomic Nervous System Regulation of Epicardial Adipose Tissue: Potential Roles for Regulator of G Protein Signaling-4.Current issues in molecular biology · 2022Review
- Cilostazol Attenuates AngII-Induced Cardiac Fibrosis in apoE Deficient Mice.International journal of molecular sciences · 2022Article
- Clinical and Molecular Implications of Osteopontin in Heart Failure.Current issues in molecular biology · 2022Review
- Regulator of G-Protein Signaling-4 Attenuates Cardiac Adverse Remodeling and Neuronal Norepinephrine Release-Promoting Free Fatty Acid Receptor FFAR3 Signaling.International journal of molecular sciences · 2022Article
- GRK5 is an essential co-repressor of the cardiac mineralocorticoid receptor and is selectively induced by finerenone.World journal of cardiology · 2022Article
- The Role of Osteopontin in Tumor Progression Through Tumor-Associated Macrophages.Frontiers in oncology · 2022Review
- Osteopontin - The stirring multifunctional regulatory factor in multisystem aging.Frontiers in endocrinology · 2022Review
- Review
- Osteopontin: The Molecular Bridge between Fat and Cardiac-Renal Disorders.International journal of molecular sciences · 2020Review
- Ubiquitin C-terminal hydrolase L1 (UCHL1) regulates post-myocardial infarction cardiac fibrosis through glucose-regulated protein of 78 kDa (GRP78).Scientific reports · 2020Article
- GRK2-Mediated Crosstalk Between β-Adrenergic and Angiotensin II Receptors Enhances Adrenocortical Aldosterone Production In Vitro and In Vivo.International journal of molecular sciences · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac β₂-adrenergic receptors (ARs) are known to inhibit collagen production and fibrosis in cardiac fibroblasts and myocytes. The β₂AR is a Gs protein-coupled receptor (GPCR) and, upon its activation, stimulates the generation of cyclic 3',5'-adenosine monophosphate (cAMP). cAMP has two effectors: protein kinase A (PKA) and the exchange protein directly activated by cAMP (Epac). Epac1 has been shown to inhibit cardiac fibroblast activation and fibrosis. Osteopontin (OPN) is a ubiquitous pro-inflammatory cytokine, which also mediates fibrosis in several tissues, including the heart. OPN underlies several cardiovascular pathologies, including atherosclerosis and cardiac adverse remodeling. We found that the cardiotoxic hormone aldosterone transcriptionally upregulates OPN in H9c2 rat cardiac myoblasts-an effect prevented by endogenous β₂AR activation. Additionally, CRISPR-mediated OPN deletion enhanced cAMP generation in response to both β₁AR and β₂AR activation in H9c2 cardiomyocytes, leading to the upregulation of Epac1 protein levels. These effects rendered β₂AR stimulation capable of completely abrogating transforming growth factor (TGF)-β-dependent fibrosis in OPN-lacking H9c2 cardiomyocytes. Finally, OPN interacted constitutively with G
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.