<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yao C</submitter><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>707-717</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7958503</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>203(6)</volume><pubmed_abstract>&lt;b>Rationale:&lt;/b> Idiopathic pulmonary fibrosis (IPF) is an insidious and fatal interstitial lung disease associated with declining pulmonary function. Accelerated aging, loss of epithelial progenitor cell function and/or numbers, and cellular senescence are implicated in the pathogenies of IPF.&lt;b>Objectives:&lt;/b> We sought to investigate the role of alveolar type 2 (AT2) cellular senescence in initiation and/or progression of pulmonary fibrosis and therapeutic potential of targeting senescence-related pathways and senescent cells.&lt;b>Methods:&lt;/b> Epithelial cells of 9 control donor proximal and distal lung tissues and 11 IPF fibrotic lung tissues were profiled by single-cell RNA sequencing to assesses the contribution of epithelial cells to the senescent cell fraction for IPF. A novel mouse</pubmed_abstract><journal>American journal of respiratory and critical care medicine</journal><pubmed_title>Senescence of Alveolar Type 2 Cells Drives Progressive Pulmonary Fibrosis.</pubmed_title><pmcid>PMC7958503</pmcid><funding_grant_id>KL2 TR001882</funding_grant_id><funding_grant_id>K08 HL141590</funding_grant_id><funding_grant_id>R01 HL135163</funding_grant_id><funding_grant_id>U01 HL110967</funding_grant_id><funding_grant_id>P01 HL108793</funding_grant_id><funding_grant_id>T32 HL134637</funding_grant_id><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Parimon T</pubmed_authors><pubmed_authors>Huang G</pubmed_authors><pubmed_authors>David G</pubmed_authors><pubmed_authors>Noble PW</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Carraro G</pubmed_authors><pubmed_authors>Weigt SS</pubmed_authors><pubmed_authors>Stripp BR</pubmed_authors><pubmed_authors>Guan X</pubmed_authors><pubmed_authors>Soukiasian HJ</pubmed_authors><pubmed_authors>Belperio JA</pubmed_authors><pubmed_authors>Yao C</pubmed_authors><pubmed_authors>Mulay A</pubmed_authors><pubmed_authors>Jiang D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Senescence of Alveolar Type 2 Cells Drives Progressive Pulmonary Fibrosis.</name><description>&lt;b>Rationale:&lt;/b> Idiopathic pulmonary fibrosis (IPF) is an insidious and fatal interstitial lung disease associated with declining pulmonary function. Accelerated aging, loss of epithelial progenitor cell function and/or numbers, and cellular senescence are implicated in the pathogenies of IPF.&lt;b>Objectives:&lt;/b> We sought to investigate the role of alveolar type 2 (AT2) cellular senescence in initiation and/or progression of pulmonary fibrosis and therapeutic potential of targeting senescence-related pathways and senescent cells.&lt;b>Methods:&lt;/b> Epithelial cells of 9 control donor proximal and distal lung tissues and 11 IPF fibrotic lung tissues were profiled by single-cell RNA sequencing to assesses the contribution of epithelial cells to the senescent cell fraction for IPF. A novel mouse</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-04T19:53:40.415Z</modification><creation>2025-04-04T19:53:40.415Z</creation></dates><accession>S-EPMC7958503</accession><cross_references><pubmed>32991815</pubmed><doi>10.1164/rccm.202004-1274OC</doi><doi>10.1164/rccm.202004-1274oc</doi></cross_references></HashMap>