FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4281484764> ?p ?o ?g. }

• W4281484764 endingPage "745" @default.
• W4281484764 startingPage "745" @default.
• W4281484764 abstract "Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension or diabetes may lead to podocyte damage, proteinuria, and rapid development of chronic kidney disease (CKD). Despite the extensive data highlighting essential functions of NO in health and pathology, related signaling in glomerular cells, particularly podocytes, is understudied. Several reports indicate that NO bioavailability in glomerular cells is decreased during the development of renal pathology, while restoring NO level can be beneficial for glomerular function. At the same time, the compromised activity of nitric oxide synthase (NOS) may provoke the formation of peroxynitrite and has been linked to autoimmune diseases such as systemic lupus erythematosus. It is known that the changes in the distribution of NO sources due to shifts in NOS subunits expression or modifications of NADPH oxidases activity may be linked to or promote the development of pathology. However, there is a lack of information about the detailed mechanisms describing the production and release of NO in the glomerular cells. The interaction of NO and other reactive oxygen species in podocytes and how NO-calcium crosstalk regulates glomerular cells' function is still largely unknown. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte. The understanding and further investigation of these essential mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that cause glomerular and kidney damage." @default.
• W4281484764 created "2022-05-26" @default.
• W4281484764 creator A5002899728 @default.
• W4281484764 creator A5023839040 @default.
• W4281484764 creator A5029940347 @default.
• W4281484764 creator A5045159645 @default.
• W4281484764 creator A5087979712 @default.
• W4281484764 date "2022-05-25" @default.
• W4281484764 modified "2023-10-17" @default.
• W4281484764 title "Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology" @default.
• W4281484764 cites W119945891 @default.
• W4281484764 cites W1503505289 @default.
• W4281484764 cites W1769943683 @default.
• W4281484764 cites W1909210290 @default.
• W4281484764 cites W1923690398 @default.
• W4281484764 cites W1966318046 @default.
• W4281484764 cites W1968216888 @default.
• W4281484764 cites W1969946612 @default.
• W4281484764 cites W1970659243 @default.
• W4281484764 cites W1972508039 @default.
• W4281484764 cites W1976019794 @default.
• W4281484764 cites W1977424733 @default.
• W4281484764 cites W1986007771 @default.
• W4281484764 cites W1997023449 @default.
• W4281484764 cites W1998378412 @default.
• W4281484764 cites W1999445997 @default.
• W4281484764 cites W2000819485 @default.
• W4281484764 cites W2000940740 @default.
• W4281484764 cites W2001045885 @default.
• W4281484764 cites W2003630942 @default.
• W4281484764 cites W2004295184 @default.
• W4281484764 cites W2004301150 @default.
• W4281484764 cites W2004490934 @default.
• W4281484764 cites W2004913283 @default.
• W4281484764 cites W2005746857 @default.
• W4281484764 cites W2007470222 @default.
• W4281484764 cites W2009700086 @default.
• W4281484764 cites W2016016054 @default.
• W4281484764 cites W2019457908 @default.
• W4281484764 cites W2020913826 @default.
• W4281484764 cites W2022466310 @default.
• W4281484764 cites W2033226277 @default.
• W4281484764 cites W2033964025 @default.
• W4281484764 cites W2036256459 @default.
• W4281484764 cites W2038381601 @default.
• W4281484764 cites W2039324204 @default.
• W4281484764 cites W2070885879 @default.
• W4281484764 cites W2077120585 @default.
• W4281484764 cites W2078027022 @default.
• W4281484764 cites W2079654264 @default.
• W4281484764 cites W2083164971 @default.
• W4281484764 cites W2085337267 @default.
• W4281484764 cites W2087828263 @default.
• W4281484764 cites W2088741178 @default.
• W4281484764 cites W2090159456 @default.
• W4281484764 cites W2099554441 @default.
• W4281484764 cites W2110062192 @default.
• W4281484764 cites W2110361956 @default.
• W4281484764 cites W2115113760 @default.
• W4281484764 cites W2119043221 @default.
• W4281484764 cites W2119712647 @default.
• W4281484764 cites W2121076246 @default.
• W4281484764 cites W2121269493 @default.
• W4281484764 cites W2123092584 @default.
• W4281484764 cites W2125319682 @default.
• W4281484764 cites W2126801791 @default.
• W4281484764 cites W2129660051 @default.
• W4281484764 cites W2132734354 @default.
• W4281484764 cites W2133150758 @default.
• W4281484764 cites W2138002856 @default.
• W4281484764 cites W2139551405 @default.
• W4281484764 cites W2146159955 @default.
• W4281484764 cites W2152381918 @default.
• W4281484764 cites W2155169902 @default.
• W4281484764 cites W2157931247 @default.
• W4281484764 cites W2161014255 @default.
• W4281484764 cites W2177647011 @default.
• W4281484764 cites W2180304435 @default.
• W4281484764 cites W2250443404 @default.
• W4281484764 cites W2286283267 @default.
• W4281484764 cites W2344962666 @default.
• W4281484764 cites W2345962527 @default.
• W4281484764 cites W2346697308 @default.
• W4281484764 cites W2463961540 @default.
• W4281484764 cites W2526436644 @default.
• W4281484764 cites W2610518686 @default.
• W4281484764 cites W2767386307 @default.
• W4281484764 cites W2767701752 @default.
• W4281484764 cites W2792589487 @default.
• W4281484764 cites W2883496301 @default.
• W4281484764 cites W2895058526 @default.
• W4281484764 cites W2911369437 @default.
• W4281484764 cites W2915749718 @default.
• W4281484764 cites W2922268276 @default.
• W4281484764 cites W2997518640 @default.
• W4281484764 cites W2998480310 @default.
• W4281484764 cites W2998590400 @default.
• W4281484764 cites W3015853957 @default.

• next