<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Han C</submitter><funding>Hui-Chun Chin and Tsung-Dao Lee Chinese Undergraduate Research Endowment</funding><funding>National Natural Science Foundation of China</funding><pagination>7006-7024</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9450841</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>59(11)</volume><pubmed_abstract>Neuroinflammation in the cardiovascular center plays a critical role in the progression of hypertensive heart disease. And microglial autophagy is involved in the regulation of neuroinflammation. Cyclic GMP-AMP synthase (cGAS), a cytosolic DNA sensor, senses mitochondrial DNA (mtDNA) and regulates autophagy. The detailed mechanisms of central cGAS affects neuroinflammatory response in hypertensive heart disease via regulating autophagy remain unknown. Angiotensin II (Ang II, 1.5 mg·kg&lt;sup>-1&lt;/sup>·12 h&lt;sup>-1&lt;/sup>, 2 weeks) was intraperitoneally injected to induce hypertension in mice. The cGAS-STING pathway was activated in the paraventricular nucleus (PVN) of Ang II-induced hypertensive mice. The contractile dysfunction of heart was alleviated in Ang II-induced hypertensive cGAS&lt;sup>-/-</pubmed_abstract><journal>Molecular neurobiology</journal><pubmed_title>Inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy.</pubmed_title><pmcid>PMC9450841</pmcid><funding_grant_id>2193101011001</funding_grant_id><funding_grant_id>No. 82171803 and No. 81770423</funding_grant_id><pubmed_authors>Qian X</pubmed_authors><pubmed_authors>Ren X</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Ooi K</pubmed_authors><pubmed_authors>Lin H</pubmed_authors><pubmed_authors>Xia C</pubmed_authors><pubmed_authors>Hu L</pubmed_authors><pubmed_authors>Han C</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Huang R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy.</name><description>Neuroinflammation in the cardiovascular center plays a critical role in the progression of hypertensive heart disease. And microglial autophagy is involved in the regulation of neuroinflammation. Cyclic GMP-AMP synthase (cGAS), a cytosolic DNA sensor, senses mitochondrial DNA (mtDNA) and regulates autophagy. The detailed mechanisms of central cGAS affects neuroinflammatory response in hypertensive heart disease via regulating autophagy remain unknown. Angiotensin II (Ang II, 1.5 mg·kg&lt;sup>-1&lt;/sup>·12 h&lt;sup>-1&lt;/sup>, 2 weeks) was intraperitoneally injected to induce hypertension in mice. The cGAS-STING pathway was activated in the paraventricular nucleus (PVN) of Ang II-induced hypertensive mice. The contractile dysfunction of heart was alleviated in Ang II-induced hypertensive cGAS&lt;sup>-/-</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-19T20:36:24.454Z</modification><creation>2025-02-19T00:35:14.489Z</creation></dates><accession>S-EPMC9450841</accession><cross_references><pubmed>36070120</pubmed><doi>10.1007/s12035-022-02994-1</doi></cross_references></HashMap>