<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xu Y</submitter><funding>Deutscher Akademischer Austauschdienst (DAAD) and University Medicine Greifswald, Anschubfinanzierung</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>National Natural Science Foundation of China</funding><funding>German Ministry of Education and Research</funding><funding>Shanghai Pujiang Program</funding><funding>Shanghai Science and Technology Innovation Natural Foundation</funding><pagination>e01175</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12412467</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(33)</volume><pubmed_abstract>Chronic kidney disease (CKD) is characterized by persistent inflammation and tubulointerstitial fibrosis leading to end-stage renal disease. Transient receptor potential canonical 6 (TRPC6) channel inhibition mitigates tubular injury and renal fibrosis in murine models of unilateral ureteral obstruction (UUO) and 2-month chronic post-ischemia-reperfusion injury (2m post-I/R). Through integrated analysis of single-cell-RNA-sequencing (scRNA-Seq) data from UUO mice treated with the selective TRPC6 inhibitor SH045, here the renoprotective cell composition and cell type-specific transcriptional programs are defined. We explored translational aspects by conducting an in-depth scRNA-Seq analysis of kidney samples from patients with CKD. These results reveal global transcriptional shifts with a d</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition.</pubmed_title><pmcid>PMC12412467</pmcid><funding_grant_id>GO766/26‐1</funding_grant_id><funding_grant_id>SFB1365</funding_grant_id><funding_grant_id>GO766/25‐1</funding_grant_id><funding_grant_id>GO766/22-2</funding_grant_id><funding_grant_id>NSFC</funding_grant_id><funding_grant_id>GO766/25-1</funding_grant_id><funding_grant_id>GO766/22‐2</funding_grant_id><funding_grant_id>GO766/26-1</funding_grant_id><funding_grant_id>GO766/18-2</funding_grant_id><funding_grant_id>GO766/18‐2</funding_grant_id><funding_grant_id>82070718</funding_grant_id><funding_grant_id>FOVB-2023-12</funding_grant_id><funding_grant_id>23ZR1451000</funding_grant_id><funding_grant_id>01GY2201</funding_grant_id><funding_grant_id>24PJD088</funding_grant_id><pubmed_authors>Zheng Z</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Schaefer M</pubmed_authors><pubmed_authors>Endlich N</pubmed_authors><pubmed_authors>Kruegel U</pubmed_authors><pubmed_authors>Oswald MS</pubmed_authors><pubmed_authors>Tsvetkov D</pubmed_authors><pubmed_authors>Simm S</pubmed_authors><pubmed_authors>Gerhardt H</pubmed_authors><pubmed_authors>Cheng G</pubmed_authors><pubmed_authors>Zhai Q</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors><pubmed_authors>Gollasch M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition.</name><description>Chronic kidney disease (CKD) is characterized by persistent inflammation and tubulointerstitial fibrosis leading to end-stage renal disease. Transient receptor potential canonical 6 (TRPC6) channel inhibition mitigates tubular injury and renal fibrosis in murine models of unilateral ureteral obstruction (UUO) and 2-month chronic post-ischemia-reperfusion injury (2m post-I/R). Through integrated analysis of single-cell-RNA-sequencing (scRNA-Seq) data from UUO mice treated with the selective TRPC6 inhibitor SH045, here the renoprotective cell composition and cell type-specific transcriptional programs are defined. We explored translational aspects by conducting an in-depth scRNA-Seq analysis of kidney samples from patients with CKD. These results reveal global transcriptional shifts with a d</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-05-29T19:42:26.584Z</modification><creation>2026-04-08T05:49:48.859Z</creation></dates><accession>S-EPMC12412467</accession><cross_references><pubmed>40525246</pubmed><doi>10.1002/advs.202501175</doi></cross_references></HashMap>