ArticleJournal of cellular and molecular medicine2020
Endothelial S1pr1 regulates pressure overload-induced cardiac remodelling through AKT-eNOS pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026Review
- Fractional carbon dioxide laser-induced photothermal activation of mesenchymal stem cell-derived exosomes accelerates diabetic wound healing by enhancing angiogenesis.World journal of diabetes · 2026Article
- Lymphatic Endothelial C-C Motif Chemokine Ligand 2 Enhances Lymphangiogenesis and Lymphatic Clearance of Macrophages Following Myocardial Infarction.Journal of the American Heart Association · 2026Article
- Molecular determinants of cardiac lymphatic dysfunction in a chronic pressure-overload model.EMBO molecular medicine · 2026Article
- Effect of exercise preconditioning on myocardial content of Sphingosine1-phosphate and its mechanism in rats after exhaustive exercise.PloS one · 2026Article
- Identification of isoliquiritigenin as a promising compound targeting lactate metabolism for heart failure alleviation.Scientific reports · 2025Article
- MARCH5 Promotes Cardiac Hypertrophy by Regulating Akt/mTOR/Gsk-3β/GATA4 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- Cardiomyocyte S1PR1 promotes cardiac regeneration via AKT/mTORC1 signaling pathway.Theranostics · 2025Article
- Zonation and ligand and dose dependence of sphingosine 1-phosphate receptor-1 signalling in blood and lymphatic vasculature.Cardiovascular research · 2024Article
- Chlorogenic acid attenuates cardiac hypertrophy via up-regulating Sphingosine-1-phosphate receptor1 to inhibit endoplasmic reticulum stress.ESC heart failure · 2024Article
- Comparative Proteomic and Phosphoproteomic Analyses Reveal Molecular Signatures of Myocardial Infarction and Transverse Aortic Constriction in Aged Mouse Models.Cardiology research and practice · 2024Article
- Deciphering transcriptional dynamics of cardiac hypertrophy and failure in a chamber-specific manner.Biomolecules & biomedicine · 2023Article
- Sphingosine-1-phosphate levels are inversely associated with left ventricular and atrial chamber volume and cardiac mass in men : The Study of Health in Pomerania (SHIP).Clinical research in cardiology : official journal of the German Cardiac Society · 2023Article
- Isorhamnetin attenuates the proliferation, invasion, migration and fibrosis of keloid fibroblasts by targeting S1PR1.Experimental and therapeutic medicine · 2023Article
- Circulating sphingolipids in heart failure.Frontiers in cardiovascular medicine · 2023Review
- Sphingosine-1-phosphate derived from PRP-Exos promotes angiogenesis in diabetic wound healing via the S1PR1/AKT/FN1 signalling pathway.Burns & trauma · 2023Article
- Endothelial-cell-mediated mechanism of coronary microvascular dysfunction leading to heart failure with preserved ejection fraction.Heart failure reviews · 2023Review
- Sphingosine-1-Phosphate Alleviates Irradiation Induced Salivary Gland Hypofunction through Preserving Endothelial Cells and Resident Macrophages.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac vascular microenvironment is crucial for cardiac remodelling during the process of heart failure. Sphingosine 1-phosphate (S1P) tightly regulates vascular homeostasis via its receptor, S1pr1. We therefore hypothesize that endothelial S1pr1 might be involved in pathological cardiac remodelling. In this study, heart failure was induced by transverse aortic constriction (TAC) operation. S1pr1 expression is significantly increased in microvascular endothelial cells (ECs) of post-TAC hearts. Endothelial-specific deletion of S1pr1 significantly aggravated cardiac dysfunction and deteriorated cardiac hypertrophy and fibrosis in myocardium. In vitro experiments demonstrated that S1P/S1pr1 praxis activated AKT/eNOS signalling pathway, leading to more production of nitric oxide (NO), which is an essential cardiac protective factor. Inhibition of AKT/eNOS pathway reversed the inhibitory effect of EC-S1pr1-overexpression on angiotensin II (AngII)-induced cardiomyocyte (CM) hypertrophy, as well as on TGF-β-mediated cardiac fibroblast proliferation and transformation towards myofibroblasts. Finally, pharmacological activation of S1pr1 ameliorated TAC-induced cardiac hypertrophy and fibrosis, leading to an improvement in cardiac function. Together, our results suggest that EC-S1pr1 might prevent the development of pressure overload-induced heart failure via AKT/eNOS pathway, and thus pharmacological activation of S1pr1 or EC-targeting S1pr1-AKT-eNOS pathway could provide a future novel therapy to improve cardiac function during heart failure development.
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