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
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