Abstract
Malaria is a parasitic disease (caused by different Plasmodium species) that affects millions of people worldwide. The lack of effective malaria drugs and a vaccine contributes to this disease, continuing to cause major public health and socioeconomic problems, especially in low-income countries. Cell death is implicated in malaria immune responses by eliminating infected cells, but it can also provoke an intense inflammatory response and lead to severe malaria outcomes. The study of the pathophysiological role of cell death in malaria in mammalians is key to understanding the parasite–host interactions and design prophylactic and therapeutic strategies for malaria. In this work, we review malaria-triggered cell death pathways (apoptosis, autophagy, necrosis, pyroptosis, NETosis, and ferroptosis) and we discuss their potential role in the development of new approaches for human malaria therapies.
Highlights
Pathways during Malaria Infection: Malaria is a parasitic disease—caused by protozoa pathogens of the Plasmodium genus—that is estimated to have infected around 228 million of people worldwide in 2018, representing a risk especially for residents of developing countries in tropical and subtropical regions [1]
External stimuli such as extracellular stress and cellular immunity activate the extrinsic pathway by providing cytokines of the TNF family, which act as death ligands, namely: Fas cell surface death receptor (FAS)-ligand (FASL), tumor necrosis factor α (TNF-α), or TNF-related apoptosis-inducing ligand (TRAIL) [58]
In studies with this species, markers indicative of LC3-II incorporating in PVM have been identified, but not the activation of BECN1; the deletion of the ATG5 gene led to the impairment of autophagy and parasites growth in hepatocytes, suggesting that the elimination of parasites occurred through a process similar to LC3-associated phagocytosis (LAP) (LAP-like) [155,156]
Summary
Pathways during Malaria Infection: Malaria is a parasitic disease—caused by protozoa pathogens of the Plasmodium genus—that is estimated to have infected around 228 million of people worldwide in 2018, representing a risk especially for residents of developing countries in tropical and subtropical regions [1] This is relevant considering underreporting, due to diagnostic difficulties in some malaria-endemic areas. Considering the above, comprehensive knowledge about the genetic, molecular, and biochemical mechanisms of the different cell death modalities has taken a prominent position in recent advances in immune response and the design of prophylactic and therapeutic methods against malaria. This infection has been reported to induce different. We review what is currently known about the distinct modalities of cell death of host cells during Plasmodium infection and the dual role of cell death in host immune protection and pathogenesis of severe malaria
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
