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The hypothalamic paraventricular nucleus (PVN) plays a central role in blood pressure (BP) regulation by modulating sympathetic tone and releasing neuropeptides that affect the cardiovascular function. In this study, we investigated the transcriptomic profile of the PVN in hypertensive strains and across sexes, aiming to identify novel sex-specific molecular pathways involved in the regulation of BP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To accomplish this goal, we sequenced RNA from the PVNs of normotensive Wistar rats and Spontaneously Hypertensive Rats (SHR), both male and female. We also performed a cardiovascular assessment based on blood pressure (BP) measurements and their variability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Cardiovascular assessment revealed higher SBP in SHRs than in Wistar rats; while males exhibited greater autonomic regulation associated with vasomotor and neurohumoral mechanisms, while females maintained comparable SBP levels primarily through an increase in heart rate, reflecting distinct autonomic adaptations. Hypertension also impacted gene expression, with influences from both the hypertensive state and sex. Compared with female SHRs, male SHRs presented a marked increase in differentially expressed genes (DEGs). Key upregulated genes in males, including\n                      <jats:italic>Brain-Derived Neurotrophic Factor (Bdnf)<\/jats:italic>\n                      and\n                      <jats:italic>Hypocretin (Hcrt)<\/jats:italic>\n                      , have already been linked to elevated BP, and\n                      <jats:italic>Angiotensin II Receptor Type 1 (Agtr1a)<\/jats:italic>\n                      is possibly associated with increased SBP-VLF variability, which serves as an indirect measure of enhanced sympathetic tone. In contrast, the female transcriptomic signature was characterized by the upregulation of anti-inflammatory pathways, with upregulation of\n                      <jats:italic>NLR Family CARD Domain Containing 3 (Nlrc3)<\/jats:italic>\n                      and\n                      <jats:italic>Paired Ig-like Receptor B (Pirb)<\/jats:italic>\n                      , and downregulation of\n                      <jats:italic>Absent in Melanoma 2 (Aim2)<\/jats:italic>\n                      , and\n                      <jats:italic>S100 Calcium Binding Protein B (S100b).<\/jats:italic>\n                      Notably, genes associated with neuroinflammation, such as the downregulation of\n                      <jats:italic>Annexin A1 (Anxa1)<\/jats:italic>\n                      and the upregulation of\n                      <jats:italic>Solute Carrier Family 11 Member 1 (Slc11a1)<\/jats:italic>\n                      , were consistently altered in both sexes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results provide new insights into the cardiovascular and molecular basis of sex differences in hypertension, suggesting distinct neurohumoral autonomic profile in males, whereas in females a greater anti-inflammatory component. These findings offer a valuable framework for developing future sex-specific therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13293-026-00855-3","type":"journal-article","created":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T13:44:35Z","timestamp":1771681475000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Sex-specific hypothalamic PVN transcriptomic signatures of blood pressure autonomic regulation and neuroinflammation in hypertension"],"prefix":"10.1186","volume":"17","author":[{"given":"V. J.","family":"Duque","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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