<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>132(21)</volume><submitter>Bao J</submitter><pubmed_abstract>Autophagy has been identified as a cellular process of bulk degradation of cytoplasmic components and its persistent activation is critically involved in the renal damage induced by ureteral obstruction. However, the role and underlying mechanisms of autophagy in hyperuricemic nephropathy (HN) remain unknown. In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-β1 (TGF-β1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. Treatment with 3-MA also abrogated the development of HN &lt;i>in vivo&lt;/i> as evidenced by improving renal function, preserving renal tissue architect</pubmed_abstract><journal>Clinical science (London, England : 1979)</journal><pagination>2299-2322</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6376616</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy.</pubmed_title><pmcid>PMC6376616</pmcid><pubmed_authors>Tao M</pubmed_authors><pubmed_authors>Bao J</pubmed_authors><pubmed_authors>Zhuang S</pubmed_authors><pubmed_authors>Liu N</pubmed_authors><pubmed_authors>Yuan W</pubmed_authors><pubmed_authors>Shi Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy.</name><description>Autophagy has been identified as a cellular process of bulk degradation of cytoplasmic components and its persistent activation is critically involved in the renal damage induced by ureteral obstruction. However, the role and underlying mechanisms of autophagy in hyperuricemic nephropathy (HN) remain unknown. In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-β1 (TGF-β1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. Treatment with 3-MA also abrogated the development of HN &lt;i>in vivo&lt;/i> as evidenced by improving renal function, preserving renal tissue architect</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Nov</publication><modification>2026-07-09T12:19:55.702Z</modification><creation>2026-07-09T11:17:27.77Z</creation></dates><accession>S-EPMC6376616</accession><cross_references><pubmed>30293967</pubmed><doi>10.1042/CS20180563</doi></cross_references></HashMap>