Key points are not available for this paper at this time.
Nanoparticles (NPs) have achieved extensive utilization across diverse domains, highlighting their unavoidable impact on health. The internalization of NPs carries the potential to trigger inflammation and instigate ailments by selectively targeting lysosomes, thereby posing significant public health concern. Lysosomes, essential organelles responsible for the degradation of biological macromolecules within cells, are crucial for cellular homeostasis and participate in key biological processes, including inter-organelle communication, signal transduction, plasma membrane repair, and immune responses. Consequently, a thorough understanding of lysosomal function is essential for elucidating the mechanisms underlying NPs-mediated toxicity. NPs-induced lysosomal dysfunction primarily involves disruptions in the acidic microenvironment of lysosomes, lysosomal membrane rupture, and membrane permeabilization. Additionally, potential molecular mechanisms contributing to the increased risk of lysosomal damage caused by NPs have been described, particularly concerning ion channel proteins such as V-ATPase, TRPM2, CLC-7, and LAMPs. This review aims to detail the alterations in lysosomal functionality induced by NPs and their associated mechanisms. By providing a theoretical framework, this review aims to support the potential application of NPs in biomedical fields.
Feng et al. (Sat,) studied this question.