{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:25:44Z","timestamp":1787027144391,"version":"build-2736575974"},"reference-count":55,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T00:00:00Z","timestamp":1775088000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Acute kidney injury (AKI) is marked by infiltration of immune cells, particularly macrophages and T cells, and their expansion as inflammatory and anti-inflammatory mediators to create a microenvironment critical for kidney injury\/repair. As the angiotensin type 2 receptor (AT\n                      <jats:sub>2<\/jats:sub>\n                      R) is emerging as reno-protective and anti-inflammatory, this study aimed to analyze the phenotypes of macrophages and helper T cells (CD4) in response to AT\n                      <jats:sub>2<\/jats:sub>\n                      R activation in ischemia-reperfusion (IR)-induced AKI.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Sprague Dawley rats were subjected to 30 min IR without and with AT2R agonist C21 administration. Rats were euthanized at 2 h, 3 d, and 5 d post IR. Flow cytometry of kidney digested cells was performed to analyze kidney infiltrating immune cells. For in-vitro polarization, mouse CD4 T cells were cultured in presence of various stimulus and characterized by flow cytometry and western blot analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      On day 3, there was a massive increase in macrophage\/monocytes (CD68\n                      <jats:sup>+<\/jats:sup>\n                      ) and M1 (CD68\n                      <jats:sup>+<\/jats:sup>\n                      CD86\n                      <jats:sup>+<\/jats:sup>\n                      ) cell accumulation and a modest increase in M2 (CD68\n                      <jats:sup>+<\/jats:sup>\n                      CD163\n                      <jats:sup>+<\/jats:sup>\n                      ) cell accumulation. The AT2R activation reduced CD68+ and M1 cells accumulation without affecting M2. Accumulation of CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD25\n                      <jats:sup>+<\/jats:sup>\n                      cells increased on day 3, and Tregs (CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD25\n                      <jats:sup>+<\/jats:sup>\n                      FoxP3\n                      <jats:sup>+<\/jats:sup>\n                      ) and Tregs-IL-10 increased at 2 h and 3 d post-IR. The AT2R agonist C21 further increased these phenotypes at all-time points. Th-17 cell accumulation increased at early time points (2 h and 3 d) but returned to normal on day 5 and was not affected by C21 treatment. Ex vivo studies revealed that AT\n                      <jats:sub>2<\/jats:sub>\n                      R agonist promoted CD4\n                      <jats:sup>+<\/jats:sup>\n                      cell expansion into Tregs, which was blocked by the AT\n                      <jats:sub>2<\/jats:sub>\n                      R antagonist PD123319, PP2A inhibitor okadaic acid, or NO synthase inhibitor L-NAME, suggesting the direct involvement of AT\n                      <jats:sub>2<\/jats:sub>\n                      R-PP2A-NOS pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      Overall, AT\n                      <jats:sub>2<\/jats:sub>\n                      R activation reduces M1 and promotes Tregs accumulation in IR-AKI, thus shifting the kidney microenvironment towards anti-inflammation and presents a potential mechanism to limit kidney injury and promote repair.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1796687","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T05:23:37Z","timestamp":1775107417000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["AT2R activation reduces M1-type macrophages and promotes tregs accumulation in ischemia-reperfusion-induced acute kidney injury"],"prefix":"10.3389","volume":"17","author":[{"given":"Riyasat","family":"Ali","sequence":"first","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, Heart and Kidney Institute, College of Pharmacy, University of Houston","place":["Houston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tahmid","family":"Faisal","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, Heart and Kidney Institute, College of Pharmacy, University of Houston","place":["Houston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kalyani","family":"Kulkarni","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, Heart and Kidney Institute, College of Pharmacy, University of Houston","place":["Houston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanket","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, Heart and Kidney Institute, College of Pharmacy, University of Houston","place":["Houston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tahir","family":"Hussain","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, Heart and Kidney Institute, College of Pharmacy, University of Houston","place":["Houston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,4,2]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"F814","DOI":"10.1152\/ajprenal.00507.2020","article-title":"Angiotensin type 2 receptor activation limits kidney injury during the early phase and induces treg cells during the late phase of renal ischemia","volume":"320","author":"Ali","year":"2021","journal-title":"Am. 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