ArticleFrontiers in pharmacology2026
AT2R activation reduces M1-type macrophages and promotes tregs accumulation in ischemia-reperfusion-induced acute kidney injury.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Protective Arm of Renin-Angiotensin System: Evidence of Nephroprotective Effects Against Acute Kidney Injury.Acta physiologica (Oxford, England) · 2026Review
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Authors and funding
5 authors.
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Abstract
Introduction: 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 Methods: 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. Results: On day 3, there was a massive increase in macrophage/monocytes (CD68 Discussion: Overall, AT
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