Wcn26-6073 Tw-37, a Blocker of Kim-1-Dependent Endocytosis, Suppresses Cellular Senescence and Associated Phenomena
Key Points
The central aim is to investigate how TW-37 impacts cellular senescence and renal fibrosis in aging-related chronic kidney disease (CKD).
Assessment of KIM-1 blockade using TW-37 in cellular models
Analysis of ACSM3 expression and collagen deposition
Investigation of epigenetic signaling pathways involved in fibrosis
TW-37 reduced markers of cellular senescence
Increased ACSM3 expression was observed
Type I collagen deposition was significantly decreased
Abstract
Importantly, KRG restored ACSM3 expression and attenuated type I collagen deposition, consistent with in vivo results. Conclusion:In conclusion, KRG alleviates renal fibrosis in agingrelated CKD by restoring ACSM3 and modulating epigenetic and profibrotic signaling.The recovery of ACSM3, accompanied by reduced H3K27ac and TGF-/Smad3 activation, represents a key molecular axis through which KRG exerts anti-fibrotic effects.These findings highlight ACSM3 as a novel molecular target of KRG and support its therapeutic potential for aging-related CKD.
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Wcn26-6073 Tw-37, a Blocker of Kim-1-Dependent Endocytosis, Suppresses Cellular Senescence and Associated Phenomena | Synapse