Key result
PGE2 signaling contributes to kidney disease outcomes that accelerate cardiovascular disease, hypertension, diabetes, and metabolic syndrome.
This review highlights the role of PGE2 signaling in kidney disease, hypertension, diabetes, and metabolic syndrome, suggesting it as a potential therapeutic target for cardiovascular risk reduction.
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Should not yet change cardiorenal management; leaves open PGE2-targeted therapies for prospective trials.
An important measure of cardiovascular health is obtained by evaluating the global cardiovascular risk, which comprises a number of factors, including hypertension and type 2 diabetes, the leading causes of illness and death in the world, as well as the metabolic syndrome. Altered immunity, inflammation, and oxidative stress underlie many of the changes associated with cardiovascular disease, diabetes, and the metabolic syndrome, and recent efforts have begun to elucidate the contribution of PGE2 in these events. This review summarizes the role of PGE2 in kidney disease outcomes that accelerate cardiovascular disease, highlights the role of cyclooxygenase-2/microsomal PGE synthase 1/PGE2 signaling in hypertension and diabetes, and outlines the contribution of PGE2 to other aspects of the metabolic syndrome, particularly abdominal adiposity, dyslipidemia, and atherogenesis. A clearer understanding of the role of PGE2 could lead to new avenues to improve therapeutic options and disease management strategies.
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Nasrallah et al. (2015) conducted a review in Cardiovascular disease, kidney disease, and metabolic syndrome. PGE2 was evaluated. PGE2 signaling contributes to kidney disease outcomes that accelerate cardiovascular disease, hypertension, diabetes, and metabolic syndrome.
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