 The study found that a specific TRPML1 agonist can reduce uranium accumulation in the kidneys, mitigate renal proximal tubular injury, increase apical exocytosis of lysosomes, and reduce lysosomal membrane permeability, LMP. This was achieved by activating the positive TRPML1-TFEB feedback loop, and consequently increasing lysosomal exocytosis and biogenesis. The study suggests that TRPML1 activation may be an effective therapeutic strategy for treating uranium-induced nephrotoxicity. This article was authored by Deng Qin Zhong, Ruoyan Wang, Hong Jing Zhong, and others.