Table 2.
Stressors triggering ASM activity and translocation (selection).
| Stressors and agonists | References | |
|---|---|---|
| Pathogens | Viral (rhinovirus, Ebola, SinbisV) | (39–42) |
| Bacterial (Neisseria gonorrhea, Staphylococcus aureus, Pseudomonas aeruginosa) | (43–49) | |
| Parasitic (Cryptosporidum parvum) | (50) | |
| Endogenous danger signals | Cytokines (IL1-β, TNF-α) | (51, 52) |
| Ligation of death receptors (TNF-α, CD95, TRAIL) | (13) | |
| Cytotoxic agents/drugs | PMA, cis-platin, paclitaxel, retinoic acid, doxorubicin | (35, 37, 53–55) |
| (Chemotherapeutics) | Rituximab | (56) |
| Radiation | UV-C, ionizing radiation | (57) |
| Oxidative stress | Ischemia/reperfusion injury | (58) |
| Generation of reactive oxygen species | (44, 45, 59) |
Outline of stressors and harmful events resulting in triggering extracellular ASM activity by translocation and exocytosis of the lysosome with decompartimentalization and amplification of biological effects of ASM at the outer leaflet of cellular membranes (selection).