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Kidney diseases, specifically acute kidney injury (AKI) and chronic kidney disease (CKD), represent major global health burdens.3,4 The pathophysiology of these renal diseases involves interconnected mechanisms, notably inflammation, fibrosis, and oxidative stress, with the excessive generation of reactive oxygen species playing a critical role in disease initiation and progression.5,6 Consequently, therapeutic strategies that modulate oxidative stress and associated redox-sensitive signaling pathways are increasingly relevant to nephrological research and clinical practice

Cell homogenate and supernatant (10 l) were transferred into a 96-well plate

Are claudin-5 tight-junction proteins in the blood-brain barrier porous

Cell 58 (21), 23592375

If it accelerates recovery beyond a natural baseline, it's a problem

doi: 10.1186/s12906017-19168 130 LaiYSChenWCHoCTLuKHLinSHTsengHCet al