Key points are not available for this paper at this time.
Despite sustained efforts, malaria elimination in developing countries, particularly in Africa, remains a to be a public burden due to the evolution and emergence of resistance to most of the currently available antimalarials and insecticides. Over time, it has been argued that a thorough understanding of the parasite's biology and pathogenesis is important because it arises from a dynamic interplay between the host and the parasite. The lifecycle of the malarial parasite is complex, involving distinct developmental stages that each express specific antigens, which in turn trigger the immune system to either protect or promote pathophysiology. Malaria pathogenesis is thus a complex interplay of Plasmodum -induced red blood cell alterations and microvascular irregularities that lead to clinical symptoms and disease severity. Immune activation during malarial infection triggers a robust production of reactive oxygen and nitrogen species (ROS/RNS), contributing to oxidative stress, a characteristic seen during malarial infection and believed to exacerbate malarial pathophysiology. Therefore, this manuscript will examine the cellular mechanism underlying malarial pathophysiology, zoom in on oxidative stress, how it is linked to malarial severity and pathophysiology, and how it could be targeted to ameliorate ROS-mediated associated complications in malaria.
Buthelezi et al. (Sat,) studied this question.