Research Paper on Signaling Involved in Podocyte Pathophysiology by Nitric Oxide

Description

Title: Signaling Involved in Podocyte Pathophysiology by Nitric Oxide

Abstract: A powerful signaling molecule involved in numerous physiological and pathophysiological processes in the kidney is nitric oxide (NO). NO has a complicated role in vasodilation, inflammation, and glomerular ultrafiltration. In pathophysiological conditions like hypertension or diabetes, changes in NO bioavailability can cause podocyte damage, proteinuria, and the rapid onset of chronic kidney disease (CKD). Despite the wealth of information highlighting the critical roles that NO plays in both health and pathology, little is known about related signaling in glomerular cells, particularly podocytes. Numerous studies show that as renal pathology progresses, NO bioavailability in glomerular cells decreases, but that raising NO levels may be advantageous for glomerular function. In addition, decreased NOS activity has been associated with autoimmune conditions like systemic lupus erythematosus and may cause the production of peroxynitrite. It is well known that changes in the distribution of NO sources caused by variations in the expression of NOS subunits or changes in the activity of NADPH oxidases may be related to or facilitate the emergence of pathology. The precise mechanisms describing the production and release of NO in the glomerular cells, however, are not well understood. There is still much to learn about how NO and other reactive oxygen species interact with podocytes and how NO-calcium crosstalk controls glomerular cell function. The understanding and further investigation of these crucial mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that result in glomerular and kidney damage. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte.

Keywords: nitric oxide synthase; glomerulus; lupus nephritis; hypertension

Paper Quality: SCOPUS / Web of Science Level Research Paper

Subject: Biomolecules

Writer Experience: 20+ Years

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