{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T04:37:48Z","timestamp":1792816668411,"version":"4.5.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T00:00:00Z","timestamp":1789084800000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>This study intends to investigate the correlation between hypertensive nephropathy (HN) and microRNA-23b-3p (miR-23b-3p) and clarify the biological function of miR-23b-3p in renal injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The serum expression levels of miR-23b-3p were compared between HN patients and healthy controls. A mouse model of HN was constructed via persistent Ang II infusion, after which the effects of miR-23b-3p on renal function (ACR\/Scr\/BUN) were examined. The mRNA levels of renal fibrosis markers (TGF-\u03b21, COL1A1, fibronectin, and \u03b1-SMA) and pro-inflammatory cytokines (TNF-\u03b1, IL-1\u03b2, and IL-6) in kidney tissues were quantified by RT-qPCR. For in vitro validation, NRK-52E cells were stimulated with Ang II. The interaction between miR-23b-3p and phosphodiesterase 4B (PDE4B) was verified using dual luciferase reporter assay and RNA pull-down assay.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In patients with HN, the expression level of miR-23b-3p was positively correlated with eGFR and negatively correlated with ACR. In the mouse model, inhibition of miR-23b-3p exacerbated renal injury; conversely, overexpression of miR-23b-3p exerted a protective effect, which was specifically manifested as decreased levels of ACR, Scr, BUN, fibrotic factors, and pro-inflammatory factors. PDE4B is a downstream target gene of miR-23b-3p. The expression trend of PDE4B was opposite to that of miR-23b-3p in HN patients, Ang II-induced mouse models, and NRK-52E cells. In NRK-52E cells, PDE4B attenuated the inhibitory effect of miR-23b-3p on fibrotic genes and inflammatory genes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The pathogenesis of HN is closely associated with the aberrant expression of miR-23b-3p. miR-23b-3p may ameliorate renal tubular fibrosis and inflammatory response via negatively regulating its target gene PDE4B.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajh\/hpag108","type":"journal-article","created":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T11:51:52Z","timestamp":1789041112000},"source":"Crossref","is-referenced-by-count":1,"title":["MiR-23b-3p exerts a protective effect in hypertensive nephropathy by inhibiting fibrosis and inflammation"],"prefix":"10.1093","author":[{"given":"Liang","family":"Fan","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Datong Modern Brain Hospital , Datong,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cunyou","family":"Xiong","sequence":"additional","affiliation":[{"name":"General Medicine, Minkang Community Health Center, Shenzhen Longhua District People\u2019s Hospital , Shenzhen,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiujuan","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kailuan General Hospital , Tangshan,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,9,11]]},"reference":[{"key":"2026102302040370500_hpag108-B1","doi-asserted-by":"publisher","first-page":"1333170","DOI":"10.3389\/fimmu.2024.1333170","article-title":"Mechanisms of inflammation modulation by different immune cells in hypertensive nephropathy","volume":"15","author":"Hao","year":"2024","journal-title":"Front Immunol"},{"key":"2026102302040370500_hpag108-B2","doi-asserted-by":"publisher","first-page":"205","DOI":"10.1097\/HJH.0000000000001170","article-title":"Hypertensive nephropathy. 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