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pf543 sphk1  (Dawley Inc)
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The role of sphingolipid metabolism in heart failure, Mechanisms and Therapeutic Targets. In the pathological process of HF, abnormal elevation of Cer can directly induces cardiomyocyte apoptosis and triggers an inflammatory response; SM and S1P, as key regulators, can attenuate the attenuate cardiac inflammation; GSL and GlcCer promote oxidative stress in cardiomyocytes, contributing to myocardial hypertrophy; DGAT1 and dhCer not only promote the accumulation of Cer, but also, together with GSL, lead to lipid deposition. These pathological changes collectively result in vascular dysfunction, myocardial fibrosis, ventricular remodeling, and disturb-ances in energy metabolism, which form the pathological basis of HF. Myriocin, an SPT inhibitor, suppresses de novo sphingolipid synthesis, reduces Cer accumulation, and alleviates apoptosis; AdipoRon lowers Cer levels and improves myocardial injury; CIN038 and Fenretinide are able to inhibit the expression of DES1, which mediates the inflammatory response in the heart; Amiselimod, an S1P receptor 1 (S1PR1) agonist, modulates S1P levels, restores endothelial ho-meostasis, and enhances vascular function; K6PC-5, an activator of <t>SPHK1,</t> increases S1P levels and ameliorates myocardial injury; and Amitriptyline, an inhibitor of aSMase, reduces endothelial inflammation by potentially slowing SM degradation.
Pf543 Sphk1, supplied by Dawley Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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The role of sphingolipid metabolism in heart failure, Mechanisms and Therapeutic Targets. In the pathological process of HF, abnormal elevation of Cer can directly induces cardiomyocyte apoptosis and triggers an inflammatory response; SM and S1P, as key regulators, can attenuate the attenuate cardiac inflammation; GSL and GlcCer promote oxidative stress in cardiomyocytes, contributing to myocardial hypertrophy; DGAT1 and dhCer not only promote the accumulation of Cer, but also, together with GSL, lead to lipid deposition. These pathological changes collectively result in vascular dysfunction, myocardial fibrosis, ventricular remodeling, and disturb-ances in energy metabolism, which form the pathological basis of HF. Myriocin, an SPT inhibitor, suppresses de novo sphingolipid synthesis, reduces Cer accumulation, and alleviates apoptosis; AdipoRon lowers Cer levels and improves myocardial injury; CIN038 and Fenretinide are able to inhibit the expression of DES1, which mediates the inflammatory response in the heart; Amiselimod, an S1P receptor 1 (S1PR1) agonist, modulates S1P levels, restores endothelial ho-meostasis, and enhances vascular function; K6PC-5, an activator of SPHK1, increases S1P levels and ameliorates myocardial injury; and Amitriptyline, an inhibitor of aSMase, reduces endothelial inflammation by potentially slowing SM degradation.

Journal: Journal of Inflammation Research

Article Title: Sphingolipid Metabolism and Signalling Pathways in Heart Failure: From Molecular Mechanism to Therapeutic Potential

doi: 10.2147/JIR.S515757

Figure Lengend Snippet: The role of sphingolipid metabolism in heart failure, Mechanisms and Therapeutic Targets. In the pathological process of HF, abnormal elevation of Cer can directly induces cardiomyocyte apoptosis and triggers an inflammatory response; SM and S1P, as key regulators, can attenuate the attenuate cardiac inflammation; GSL and GlcCer promote oxidative stress in cardiomyocytes, contributing to myocardial hypertrophy; DGAT1 and dhCer not only promote the accumulation of Cer, but also, together with GSL, lead to lipid deposition. These pathological changes collectively result in vascular dysfunction, myocardial fibrosis, ventricular remodeling, and disturb-ances in energy metabolism, which form the pathological basis of HF. Myriocin, an SPT inhibitor, suppresses de novo sphingolipid synthesis, reduces Cer accumulation, and alleviates apoptosis; AdipoRon lowers Cer levels and improves myocardial injury; CIN038 and Fenretinide are able to inhibit the expression of DES1, which mediates the inflammatory response in the heart; Amiselimod, an S1P receptor 1 (S1PR1) agonist, modulates S1P levels, restores endothelial ho-meostasis, and enhances vascular function; K6PC-5, an activator of SPHK1, increases S1P levels and ameliorates myocardial injury; and Amitriptyline, an inhibitor of aSMase, reduces endothelial inflammation by potentially slowing SM degradation.

Article Snippet: PF543 , SPHK1 , Suppresses inflammation, reduces cardiomyocyte hypertrophy, and promotes cardiac remodeling , 4 weeks , Myocardial infarction , Sprague-Dawley rats , No.

Techniques: Biomarker Discovery, Expressing

Drugs Targeting Sphingolipid Metabolism and Their Effect on HF

Journal: Journal of Inflammation Research

Article Title: Sphingolipid Metabolism and Signalling Pathways in Heart Failure: From Molecular Mechanism to Therapeutic Potential

doi: 10.2147/JIR.S515757

Figure Lengend Snippet: Drugs Targeting Sphingolipid Metabolism and Their Effect on HF

Article Snippet: PF543 , SPHK1 , Suppresses inflammation, reduces cardiomyocyte hypertrophy, and promotes cardiac remodeling , 4 weeks , Myocardial infarction , Sprague-Dawley rats , No.

Techniques: