<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kuwabara JT</submitter><funding>Naito Foundation</funding><funding>American Heart Association</funding><funding>Paul G. Allen Frontiers Group</funding><funding>NHLBI NIH HHS</funding><funding>NIMHD NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><funding>Japan Society for the Promotion of Science</funding><pagination>e69854</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9576271</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><pubmed_abstract>Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. Although fibrosis accompanies many cardiac pathologies and is generally deleterious, the role of fibroblasts in maintaining the basal ECM network and in fibrosis in vivo is poorly understood. We genetically ablated fibroblasts in mice to evaluate the impact on homeostasis of adult ECM and cardiac function after injury. Fibroblast-ablated mice demonstrated a substantive reduction in cardiac fibroblasts, but fibrillar collagen and the ECM proteome were not overtly altered when evaluated by quantitative mass spectrometry and N-terminomics. However, the distribution and quantity of collagen VI, microfibrillar collagen that forms an open network with the basement membrane, </pubmed_abstract><journal>eLife</journal><pubmed_title>Consequences of PDGFRα&lt;sup>+&lt;/sup> fibroblast reduction in adult murine hearts.</pubmed_title><pmcid>PMC9576271</pmcid><funding_grant_id>T32 HL115505</funding_grant_id><funding_grant_id>R01 HL074257</funding_grant_id><funding_grant_id>G12 MD007601</funding_grant_id><funding_grant_id>P30 GM103341</funding_grant_id><funding_grant_id>PRE29630019</funding_grant_id><funding_grant_id>PRE834732</funding_grant_id><funding_grant_id>GRNT33660474</funding_grant_id><funding_grant_id>HL074257</funding_grant_id><funding_grant_id>S10 OD023436</funding_grant_id><funding_grant_id>HL115505</funding_grant_id><funding_grant_id>S10 OD028515</funding_grant_id><funding_grant_id>P30 CA071789</funding_grant_id><pubmed_authors>Hara A</pubmed_authors><pubmed_authors>Lee AY</pubmed_authors><pubmed_authors>Ziolo MT</pubmed_authors><pubmed_authors>Bhutada S</pubmed_authors><pubmed_authors>Apte SS</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Kuwabara JT</pubmed_authors><pubmed_authors>Gojanovich GS</pubmed_authors><pubmed_authors>Hokutan K</pubmed_authors><pubmed_authors>Shettigar V</pubmed_authors><pubmed_authors>Heckl JR</pubmed_authors><pubmed_authors>DeAngelo LP</pubmed_authors><pubmed_authors>Jahansooz JR</pubmed_authors><pubmed_authors>Tacdol DK</pubmed_authors><pubmed_authors>Tallquist MD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Consequences of PDGFRα&lt;sup>+&lt;/sup> fibroblast reduction in adult murine hearts.</name><description>Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. Although fibrosis accompanies many cardiac pathologies and is generally deleterious, the role of fibroblasts in maintaining the basal ECM network and in fibrosis in vivo is poorly understood. We genetically ablated fibroblasts in mice to evaluate the impact on homeostasis of adult ECM and cardiac function after injury. Fibroblast-ablated mice demonstrated a substantive reduction in cardiac fibroblasts, but fibrillar collagen and the ECM proteome were not overtly altered when evaluated by quantitative mass spectrometry and N-terminomics. However, the distribution and quantity of collagen VI, microfibrillar collagen that forms an open network with the basement membrane, </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2025-04-27T03:35:02.929Z</modification><creation>2025-04-06T18:55:03.176Z</creation></dates><accession>S-EPMC9576271</accession><cross_references><pubmed>36149056</pubmed><doi>10.7554/eLife.69854</doi></cross_references></HashMap>