Matches in SemOpenAlex for { <https://semopenalex.org/work/W2186352307> ?p ?o ?g. }
- W2186352307 abstract "Introduction Cyclic guanosine monophosphate (cGMP) signaling plays a critical role in physiological homeostatic processes such as smooth muscle tone in vascular and non-vascular tissues, platelet activity, cardiac contractility, renal function and fluid balance, as well as cell growth. The cGMP signaling consists of cGMP-generating guanylyl-cyclases, protein kinases, phosphodiesterases, endopeptidases, ion channel and efflux transporters and hence substances that increase cGMP levels are important targets for the treatment of cardiovascular and non-vascular-related diseases. Studies of the 90’s established endothelium dysfunction as one of the major causes of cardiovascular diseases and therapeutic strategies that benefit NO bioavailability have been applied in clinical medicine extensively. Recently, the basic and clinical studies of cGMP regulation through either activation of particulate guanylyl cyclase (pGC) and soluble guanylyl cyclase (sGC) or inhibition of cyclic nucleotide phosphodiesterase type 5 (PDE5) have resulted in effective therapies for congestive heart failure, pulmonary hypertension, erectile dysfunction and more recently for benign prostatic hyperplasia. This review highlights pharmacological aspects of sGC and pGC activation and PDE5 inhibition in the treatment of cardiovascular (heart failure and pulmonary hypertension) and vascular-related diseases (erectile dysfunction and lower urinary tract symptoms secondary to benign prostatic hyperplasia). Conclusion The discovery of the NO-cGMP pathway revolutionized the comprehension of pathophysiological mechanisms involved on cardiovascular diseases. However, considering the expression “from bench to bedside”, the therapeutic alternatives that target NO-cGMP did not immediately follow the biochemical and pathophysiological revolution since few therapeutic options have been proven effective and released on the market for the treatment of cardiovascular disorders." @default.
- W2186352307 created "2016-06-24" @default.
- W2186352307 creator A5015836787 @default.
- W2186352307 creator A5044158442 @default.
- W2186352307 creator A5066062695 @default.
- W2186352307 date "2014-01-01" @default.
- W2186352307 modified "2023-09-27" @default.
- W2186352307 title "Modulating cGMP levels as therapeutic drug targets in cardiovascular and non-cardiovascular diseases" @default.
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