Preclinical study demonstrates that AT2R agonist C21 prevents tubular damage in renal ischemia-reperfusion by preserving primary cilia, highlighting a protective target in acute kidney injury.
AT2R agonist C21 elicits nephroprotective effects in ischemia/reperfusion (IR)-induced acute kidney injury (AKI) by preventing tubular cell damage. IR-induced AKI associates with tubular cell deciliation. Primary cilia are sensory organelles that regulate signaling pathways central for tubular cell survival, whose stability depends on α-tubulin acetylation. Extracellular signal-regulated kinases (ERK) activates Histone-deacetylase 6 (HDAC6), which is the main α-tubulin deacetylase involved in loss of primary cilia stability in epithelial cells.
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Maknis et al. (2024) studied this question.
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