These pathological processes are intertwined, forming a vicious cycle of energy depletion-oxidative stress-inflammatory response-cell death-microcirculatory dysfunction, which not only causes AKI but also accelerates the progression of chronic pathologies such as renal interstitial fibrosis, significantly impacting prognosis and clinical outcomes [47, 48]
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Its core proposed mechanism is the sequestering of G-actin, which influences the cell migration central to tissue repair, alongside preclinical links to angiogenesis and reduced inflammation