<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Alvarez-Heredia P</submitter><funding>Fundación para la Investigación Biomédica de Córdoba</funding><funding>European Union's Horizon 2020 research and innovation program under the Marie Skłodow-ska-Curie "</funding><funding>Instituto de Salud Carlos III</funding><funding>Regional Ministry of Economic Transformation, Industry, Knowledge, and Universities of the Junta de Andalucía, co-financed by the European Union through the European Social Fund "The ESF invests in your future"</funding><funding>Consejería de salud y familias Junta de Andalucía, Subvenciones para la financiación de la I+D+i biomédica y en ciencias de la salud en Andalucía 2021, co-funded by European Union (FEDER Andalucía 2014-2020)</funding><pagination>2194</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9916774</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(3)</volume><pubmed_abstract>Aortic stenosis (AS) is a frequent cardiac disease in old individuals, characterized by valvular calcification, fibrosis, and inflammation. Recent studies suggest that AS is an active inflammatory atherosclerotic-like process. Particularly, it has been suggested that several immune cell types, present in the valve infiltrate, contribute to its degeneration and to the progression toward stenosis. Furthermore, the infiltrating T cell subpopulations mainly consist of oligoclonal expansions, probably specific for persistent antigens. Thus, the characterization of the cells implicated in the aortic valve calcification and the analysis of the antigens to which those cells respond to is of utmost importance to develop new therapies alternative to the replacement of the valve itself. However, calc</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>A Straightforward Cytometry-Based Protocol for the Comprehensive Analysis of the Inflammatory Valve Infiltrate in Aortic Stenosis.</pubmed_title><pmcid>PMC9916774</pmcid><funding_grant_id>PI-0324-2018</funding_grant_id><funding_grant_id>PI1900075</funding_grant_id><funding_grant_id>DOC_01421</funding_grant_id><funding_grant_id>PE-COVID-0053-2020</funding_grant_id><funding_grant_id>847468</funding_grant_id><pubmed_authors>Munoz I</pubmed_authors><pubmed_authors>Alvarez-Heredia P</pubmed_authors><pubmed_authors>Lopez-Romero R</pubmed_authors><pubmed_authors>Dominguez-Del-Castillo JJ</pubmed_authors><pubmed_authors>Batista-Duharte A</pubmed_authors><pubmed_authors>Trujillo-Aguilera A</pubmed_authors><pubmed_authors>Gutierrez-Gonzalez C</pubmed_authors><pubmed_authors>Hassouneh F</pubmed_authors><pubmed_authors>Solana R</pubmed_authors><pubmed_authors>Pera A</pubmed_authors><pubmed_authors>Reina-Alfonso I</pubmed_authors></additional><is_claimable>false</is_claimable><name>A Straightforward Cytometry-Based Protocol for the Comprehensive Analysis of the Inflammatory Valve Infiltrate in Aortic Stenosis.</name><description>Aortic stenosis (AS) is a frequent cardiac disease in old individuals, characterized by valvular calcification, fibrosis, and inflammation. Recent studies suggest that AS is an active inflammatory atherosclerotic-like process. Particularly, it has been suggested that several immune cell types, present in the valve infiltrate, contribute to its degeneration and to the progression toward stenosis. Furthermore, the infiltrating T cell subpopulations mainly consist of oligoclonal expansions, probably specific for persistent antigens. Thus, the characterization of the cells implicated in the aortic valve calcification and the analysis of the antigens to which those cells respond to is of utmost importance to develop new therapies alternative to the replacement of the valve itself. However, calc</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-06-01T03:58:01.084Z</modification><creation>2024-11-19T19:01:33.707Z</creation></dates><accession>S-EPMC9916774</accession><cross_references><pubmed>36768515</pubmed><doi>10.3390/ijms24032194</doi></cross_references></HashMap>