{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T08:29:40Z","timestamp":1777624180175,"version":"3.51.4"},"reference-count":34,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,23]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec id=\"j_med-2026-1412_abs_002\">\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To investigate the causal relationship between genetically predicted levels of five circulating cytokines\u00a0\u2013\u00a0CXCL11, IL-2, IL-4, leukemia inhibitory factor (LIF), and neurotrophin-3 (NT-3)\u00a0\u2013\u00a0and the risk of hypertensive encephalopathy using a two-sample Mendelian randomization (MR) approach.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_med-2026-1412_abs_003\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Single nucleotide polymorphisms (SNPs) strongly associated with each cytokine (p\n                      <jats:italic>&lt;<\/jats:italic>\n                      5\u00a0\u00d7\u00a010\n                      <jats:sup>\u22128<\/jats:sup>\n                      ) were selected from publicly available GWAS data. Summary statistics for HE were obtained from the FinnGen biobank (endpoint: I9_HYPERTENC). MR analyses were conducted using inverse-variance weighted (IVW), MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses included heterogeneity testing, MR-Egger intercept assessment, and leave-one-out analysis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_med-2026-1412_abs_004\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Genetically higher levels of IL-2 (OR=0.35, 95\u202f% CI: 0.13\u20130.99, p\n                      <jats:italic>=<\/jats:italic>\n                      0.043), IL-4 (OR=0.50, 95\u202f% CI: 0.30\u20130.85, p\n                      <jats:italic>=<\/jats:italic>\n                      0.010), and NT-3 (OR=0.46, 95\u202f% CI: 0.28\u20130.75, p\n                      <jats:italic>=<\/jats:italic>\n                      0.0038) were significantly associated with lower risk of HE. CXCL11 showed a significant positive association with HE risk (OR=2.79, 95\u202f% CI: 1.26\u20136.20, p\n                      <jats:italic>=<\/jats:italic>\n                      0.028). LIF displayed a non-significant trend toward protection (OR=0.43, p\n                      <jats:italic>=<\/jats:italic>\n                      0.060). Results were consistent across sensitivity analyses with no evidence of pleiotropy or heterogeneity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_med-2026-1412_abs_006\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This Mendelian randomization study provides evidence that genetically determined levels of IL-2, IL-4, and NT-3 are protective against hypertensive encephalopathy, while CXCL11 is a risk factor. These cytokines may serve as potential biomarkers or therapeutic targets for HE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1515\/med-2026-1412","type":"journal-article","created":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T20:57:05Z","timestamp":1777409825000},"source":"Crossref","is-referenced-by-count":0,"title":["The causal relationship in hypertensive encephalopathy: mechanistic analysis of five specific circulating cytokines"],"prefix":"10.1515","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-5127-5311","authenticated-orcid":false,"given":"Pengfei","family":"Zhang","sequence":"first","affiliation":[{"name":"School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University , Nangchang , China"},{"name":"School of Queen Mary, Jiangxi Medical College, Nanchang University Nanchang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-7771-462X","authenticated-orcid":false,"given":"Yijia","family":"Huang","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University , Nangchang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haoying","family":"Li","sequence":"additional","affiliation":[{"name":"School of Queen Mary, Jiangxi Medical College, Nanchang University Nanchang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-9234-6752","authenticated-orcid":false,"given":"Can","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University , Nangchang , China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhiren","family":"Chen","sequence":"additional","affiliation":[{"name":"XuZhou Central Hospital , Xuzhou , China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2026,4,24]]},"reference":[{"key":"2026042823132714160_j_med-2026-1412_ref_001","doi-asserted-by":"crossref","unstructured":"van den Born, BH, Lip, GYH, Brguljan-Hitij, J, Cremer, A, Segura, J, Morales, E, et al.. 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