sphingosine-1-phosphate has been researched along with Malaria* in 2 studies
2 review(s) available for sphingosine-1-phosphate and Malaria
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Malaria link of hypertension: a hidden syndicate of angiotensin II, bradykinin and sphingosine 1-phosphate.
In malaria-endemic countries, the burden of hypertension is on the rise. Although malaria and hypertension seem to have no direct link, several studies in recent years support their possible link. Three bioactive molecules such as angiotensin II (Ang II), bradykinin (BK) and sphingosine 1-phosphate (S1P) are crucial in regulating blood pressure. While the increased level of Ang II and S1P are responsible for inducing hypertension, BK is arthero-protective and anti-hypertensive. Therefore, in the present review, based on available literatures we highlight the present knowledge on the production and bioavailability of these molecules, the mechanism of their regulation of hypertension, and patho-physiological role in malaria. Further, a possible link between malaria and hypertension is hypothesized through various arguments based on experimental evidence. Understanding of their mechanisms of blood pressure regulation during malaria infection may open up avenues for drug therapeutics and management of malaria in co-morbidity with hypertension. Topics: Angiotensin II; Blood Pressure; Bradykinin; Comorbidity; Female; Humans; Hypertension; Lysophospholipids; Malaria; Male; Pregnancy; Sphingosine | 2021 |
Sphingosine 1-Phosphate in Malaria Pathogenesis and Its Implication in Therapeutic Opportunities.
Sphingosine 1-Phosphate (S1P) is a bioactive lipid intermediate in the sphingolipid metabolism, which exist in two pools, intracellular and extracellular, and each pool has a different function. The circulating extracellular pool, specifically the plasma S1P is shown to be important in regulating various physiological processes related to malaria pathogenesis in recent years. Although blood cells (red blood cells and platelets), vascular endothelial cells and hepatocytes are considered as the important sources of plasma S1P, their extent of contribution is still debated. The red blood cells (RBCs) and platelets serve as a major repository of intracellular S1P due to lack, or low activity of S1P degrading enzymes, however, contribution of platelets toward maintaining plasma S1P is shown negligible under normal condition. Substantial evidences suggest platelets loss during Topics: Endothelial Cells; Humans; Lysophospholipids; Malaria; Sphingosine | 2020 |