Sickle cell anemia (SCA) is a hereditary blood disorder characterized by the presence of abnormal hemoglobin, leading to
the formation of sickle-shaped red blood cells. While much research has focused on the molecular and cellular mechanisms
underlying the pathophysiology of SCA, recent attention has turned to the role of apoptosis, or programmed cell death, in
the disease progression. This review aims to elucidate the intricate mechanisms of apoptosis in SCA patients and explore its
implications in disease severity, complications, and potential therapeutic interventions. Different research search engines such
as PubMed central, Scopus, Web of Science, Google Scholar, ResearchGate, Academia Edu, etc were utilized in writing this
paper. Apoptosis, a highly regulated cellular process, plays a crucial role in maintaining homeostasis by eliminating damaged or
dysfunctional cells. In SCA, the imbalance between pro-apoptotic and anti-apoptotic signals contributes to increased erythrocyte
apoptosis, exacerbating anemia and vaso-occlusive crises. Various factors, including oxidative stress, inflammation, and altered
cell signaling pathways, converge to modulate the apoptotic response in SCA. Furthermore, the interaction between apoptotic
cells and the vascular endothelium contributes to endothelial dysfunction, promoting the pathogenesis of vasculopathy and organ
damage seen in SCA patients. In conclusion, unraveling the complexities of apoptosis in SCA provides valuable insights into the
disease pathophysiology and offers novel avenues for therapeutic interventions.
Abbreviations: DAMPs = damage-associated molecular patterns, HbS = hemoglobin S, SCA = sickle cell anemia.
Keywords: apoptosis, inflammation, reactive oxygen species, sickle cell anemia, vaso-occlusive crises