<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Garchow B</submitter><funding>National Institute of Arthritis and Musculoskeletal and Skin Diseases</funding><funding>Thomas Jefferson University</funding><funding>NIAMS NIH HHS</funding><pagination>128-134</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8026684</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>133</volume><pubmed_abstract>Systemic lupus erythematosus (SLE, lupus) is a chronic autoimmune disease characterized by loss of peripheral tolerance to nuclear self-antigens. It is increasingly recognized that aberrant T cell metabolism is a critical mediator of SLE immunopathology. Hypoxia inducible factor 1⍺ (HIF-1α) is a key transcription factor that regulates T cell metabolism in response to immune stimuli. T cell activation induces HIF-1α expression and transcriptional activation of HIF-responsive genes. HypoxamiRs are a group of microRNAs sensitive to HIF-1α transcriptional regulation that function to fine-tune the HIF-driven transcriptional program. The 'master' hypoxamiR, miR-210 is transcriptionally regulated by HIF-1α and negatively regulates HIF-1α activity. Although a key role for HIF-1α in has been descri</pubmed_abstract><journal>Molecular immunology</journal><pubmed_title>HIF-1α and miR-210 differential and lineage-specific expression in systemic lupus erythematosus.</pubmed_title><pmcid>PMC8026684</pmcid><funding_grant_id>R03 AR060988</funding_grant_id><funding_grant_id>R21 AR063416</funding_grant_id><pubmed_authors>Kiriakidou M</pubmed_authors><pubmed_authors>Maque Acosta Y</pubmed_authors><pubmed_authors>Garchow B</pubmed_authors></additional><is_claimable>false</is_claimable><name>HIF-1α and miR-210 differential and lineage-specific expression in systemic lupus erythematosus.</name><description>Systemic lupus erythematosus (SLE, lupus) is a chronic autoimmune disease characterized by loss of peripheral tolerance to nuclear self-antigens. It is increasingly recognized that aberrant T cell metabolism is a critical mediator of SLE immunopathology. Hypoxia inducible factor 1⍺ (HIF-1α) is a key transcription factor that regulates T cell metabolism in response to immune stimuli. T cell activation induces HIF-1α expression and transcriptional activation of HIF-responsive genes. HypoxamiRs are a group of microRNAs sensitive to HIF-1α transcriptional regulation that function to fine-tune the HIF-driven transcriptional program. The 'master' hypoxamiR, miR-210 is transcriptionally regulated by HIF-1α and negatively regulates HIF-1α activity. Although a key role for HIF-1α in has been descri</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2025-04-27T01:39:44.537Z</modification><creation>2025-04-06T18:20:47.179Z</creation></dates><accession>S-EPMC8026684</accession><cross_references><pubmed>33657462</pubmed><doi>10.1016/j.molimm.2021.02.019</doi></cross_references></HashMap>