<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kiss T</submitter><funding>BLRD VA</funding><funding>NEI NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><funding>National Institute on Aging</funding><pagination>953-981</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9135944</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>44(2)</volume><pubmed_abstract>Vascular aging has a central role in the pathogenesis of cardiovascular diseases contributing to increased mortality of older adults. There is increasing evidence that, in addition to the documented role of cell-autonomous mechanisms of aging, cell-nonautonomous mechanisms also play a critical role in the regulation of vascular aging processes. Our recent transcriptomic studies (Kiss T. et al. Geroscience. 2020;42(2):727-748) demonstrated that circulating anti-geronic factors from young blood promote vascular rejuvenation in aged mice. The present study was designed to expand upon the results of this study by testing the hypothesis that circulating pro-geronic factors also contribute to the genesis of vascular aging phenotypes. To test this hypothesis, through heterochronic parabiosis, we </pubmed_abstract><journal>GeroScience</journal><pubmed_title>Old blood from heterochronic parabionts accelerates vascular aging in young mice: transcriptomic signature of pathologic smooth muscle remodeling.</pubmed_title><pmcid>PMC9135944</pmcid><funding_grant_id>U54 GM104938</funding_grant_id><funding_grant_id>P30 EY001792</funding_grant_id><funding_grant_id>R01AG070915</funding_grant_id><funding_grant_id>T32 AG052363</funding_grant_id><funding_grant_id>R01 AG068295</funding_grant_id><funding_grant_id>R01 AG055395</funding_grant_id><funding_grant_id>K01 AG073614</funding_grant_id><funding_grant_id>K01AG073614</funding_grant_id><funding_grant_id>P20 GM125528</funding_grant_id><funding_grant_id>RF1 AG072295</funding_grant_id><funding_grant_id>I01 BX005592</funding_grant_id><funding_grant_id>P30AG050911</funding_grant_id><funding_grant_id>P30 GM110766</funding_grant_id><funding_grant_id>R01 EY010609</funding_grant_id><funding_grant_id>T32AG052363</funding_grant_id><funding_grant_id>R01AG055395</funding_grant_id><funding_grant_id>R01 NS100782</funding_grant_id><funding_grant_id>P30AG038072</funding_grant_id><funding_grant_id>P30 AG050911</funding_grant_id><funding_grant_id>P30 AG038072</funding_grant_id><funding_grant_id>R01 CA255840</funding_grant_id><funding_grant_id>P20 GM103447</funding_grant_id><funding_grant_id>R01 AG070915</funding_grant_id><funding_grant_id>R01AG068295</funding_grant_id><funding_grant_id>RF1AG072295</funding_grant_id><pubmed_authors>Benyo Z</pubmed_authors><pubmed_authors>Garman L</pubmed_authors><pubmed_authors>Yabluchanskiy A</pubmed_authors><pubmed_authors>Kiss T</pubmed_authors><pubmed_authors>Balasubramanian P</pubmed_authors><pubmed_authors>Mukli P</pubmed_authors><pubmed_authors>Ungvari Z</pubmed_authors><pubmed_authors>Tarantini S</pubmed_authors><pubmed_authors>Csiszar A</pubmed_authors><pubmed_authors>Ungvari A</pubmed_authors><pubmed_authors>Nyul-Toth A</pubmed_authors><pubmed_authors>Gulej R</pubmed_authors><pubmed_authors>Csipo T</pubmed_authors><pubmed_authors>Conley SM</pubmed_authors><pubmed_authors>Huffman DM</pubmed_authors><pubmed_authors>Wren JD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Old blood from heterochronic parabionts accelerates vascular aging in young mice: transcriptomic signature of pathologic smooth muscle remodeling.</name><description>Vascular aging has a central role in the pathogenesis of cardiovascular diseases contributing to increased mortality of older adults. There is increasing evidence that, in addition to the documented role of cell-autonomous mechanisms of aging, cell-nonautonomous mechanisms also play a critical role in the regulation of vascular aging processes. Our recent transcriptomic studies (Kiss T. et al. Geroscience. 2020;42(2):727-748) demonstrated that circulating anti-geronic factors from young blood promote vascular rejuvenation in aged mice. The present study was designed to expand upon the results of this study by testing the hypothesis that circulating pro-geronic factors also contribute to the genesis of vascular aging phenotypes. To test this hypothesis, through heterochronic parabiosis, we </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2026-05-07T03:17:43.719Z</modification><creation>2025-02-19T02:59:10.483Z</creation></dates><accession>S-EPMC9135944</accession><cross_references><pubmed>35124764</pubmed><doi>10.1007/s11357-022-00519-1</doi></cross_references></HashMap>