Macrophage AMPK activated by oxidative stress drives profibrotic crosstalk with tubular cells to accelerate renal fibrosis after ischemic and reperfusion injury.

Redox Biol · 2026 · PMC12882646 · PMID 41621245

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a decreasing trendno p-value reported

The results identified that AMPK phosphorylation was preferentially induced by H 2 O 2 and hypoxia, but was unaltered by IL-6 and showed a decreasing trend with TGF-β stimulation ( Fig. 2 F and G).

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