RESUMO
An investigation of the potential role of lysosomes in airborne particulate matter (APM) induced health risks is essential to fully comprehend the pathogenic mechanisms of respiratory diseases. It is commonly accepted that APM-induced lung injury is caused by oxidative stress, inflammatory responses, and DNA damage. In addition, there exists abundant evidence that changes in lysosomal function are essential for cellular adaptation to a variety of particulate stimuli. This review emphasizes that disruption of the lysosomal structure/function is a key step in the cellular metabolic imbalance induced by APMs. After being ingested by cells, most particles are localized within lysosomes. Thus, lysosomes become the primary locus where APMs accumulate, and here they undergo degradation and release toxic components. Recent studies have provided incontrovertible evidence that a wide variety of APMs interfere with the normal function of lysosomes. After being stimulated by APMs, lysosome rupture leads to a loss of lysosomal acidic conditions and the inactivation of proteolytic enzymes, promoting an inflammatory response by activating the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Moreover, APMs interfere with autophagosome production or block autophagic flux, resulting in autophagy dysfunction. Additionally, APMs disrupt the normal function of lysosomes in iron metabolism, leading to disruption on iron homeostasis. Therefore, understanding the impacts of APM exposure from the perspective of lysosomes will provide new insights into the detrimental consequences of air pollution.
