{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T22:02:14Z","timestamp":1781215334548,"version":"3.54.1"},"reference-count":260,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T00:00:00Z","timestamp":1683849600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH","award":["DK116591"],"award-info":[{"award-number":["DK116591"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>Diabetic nephropathy (DN) remains the leading cause of vascular morbidity and mortality in diabetes patients. Despite the progress in understanding the diabetic disease process and advanced management of nephropathy, a number of patients still progress to end-stage renal disease (ESRD). The underlying mechanism still needs to be clarified. Gaseous signaling molecules, so-called gasotransmitters, such as nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), have been shown to play an essential role in the development, progression, and ramification of DN depending on their availability and physiological actions. Although the studies on gasotransmitter regulations of DN are still emerging, the evidence revealed an aberrant level of gasotransmitters in patients with diabetes. In studies, different gasotransmitter donors have been implicated in ameliorating diabetic renal dysfunction. In this perspective, we summarized an overview of the recent advances in the physiological relevance of the gaseous molecules and their multifaceted interaction with other potential factors, such as extracellular matrix (ECM), in the severity modulation of DN. Moreover, the perspective of the present review highlights the possible therapeutic interventions of gasotransmitters in ameliorating this dreaded disease.<\/jats:p>","DOI":"10.3390\/antiox12051088","type":"journal-article","created":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T09:26:13Z","timestamp":1683883573000},"page":"1088","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Diabetic Nephropathy and Gaseous Modulators"],"prefix":"10.3390","volume":"12","author":[{"given":"Subir Kumar","family":"Juin","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Louisville School of Medicine, Louisville, KY 40202, USA"},{"name":"Department of Microbiology & Immunology, Brown Cancer Center, Center for Microbiomics, Inflammation and Pathogenicity, University of Louisville School of Medicine, Louisville, KY 40202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosemary","family":"Ouseph","sequence":"additional","affiliation":[{"name":"Division of Nephrology & Hypertension, University of Louisville School of Medicine, Louisville, KY 40202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dibson Dibe","family":"Gondim","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Louisville School of Medicine, Louisville, KY 40202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4206-7305","authenticated-orcid":false,"given":"Venkatakrishna Rao","family":"Jala","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Brown Cancer Center, Center for Microbiomics, Inflammation and Pathogenicity, University of Louisville School of Medicine, Louisville, KY 40202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Utpal","family":"Sen","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Louisville School of Medicine, Louisville, KY 40202, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,5,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"172","DOI":"10.1016\/j.niox.2015.02.003","article-title":"MMP-9- and NMDA receptor-mediated mechanism of diabetic renovascular remodeling and kidney dysfunction: Hydrogen sulfide is a key modulator","volume":"46","author":"Kundu","year":"2015","journal-title":"Nitric Oxide"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"S94","DOI":"10.2337\/diacare.26.2007.S94","article-title":"Diabetic nephropathy","volume":"26","author":"Molitch","year":"2003","journal-title":"Diabetes Care"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"1238","DOI":"10.2337\/diabetes.54.4.1238","article-title":"Genetic variation at the ACE gene is associated with persistent microalbuminuria and severe nephropathy in type 1 diabetes: The DCCT\/EDIC Genetics Study","volume":"54","author":"Boright","year":"2005","journal-title":"Diabetes"},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"106030","DOI":"10.1016\/j.phrs.2021.106030","article-title":"Toll-like receptor 4 mutation protects the kidney from Ang-II-induced hypertensive injury","volume":"175","author":"Majumder","year":"2022","journal-title":"Pharmacol. 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