Publications

Sickle cell anemia (SCA) is a hereditary blood disorder characterized by the presence of abnormal hemoglobin, leading tothe formation of sickle-shaped red blood cells. While much research has focused on the molecular and cellular mechanismsunderlying the pathophysiology of SCA, recent attention has turned to the role of apoptosis, or programmed cell death, inthe disease progression. This review aims to elucidate the intricate mechanisms of apoptosis in SCA patients and explore itsimplications in disease severity, complications, and potential therapeutic interventions. Different research search engines suchas PubMed central, Scopus, Web of Science, Google Scholar, ResearchGate, Academia Edu, etc were utilized in writing thispaper. Apoptosis, a highly regulated cellular process, plays a crucial role in maintaining homeostasis by eliminating damaged ordysfunctional cells. In SCA, the imbalance between pro-apoptotic and anti-apoptotic signals contributes to increased erythrocyteapoptosis, exacerbating anemia and vaso-occlusive crises. Various factors, including oxidative stress, inflammation, and alteredcell signaling pathways, converge to modulate the apoptotic response in SCA. Furthermore, the interaction between apoptoticcells and the vascular endothelium contributes to endothelial dysfunction, promoting the pathogenesis of vasculopathy and organdamage seen in SCA patients. In conclusion, unraveling the complexities of apoptosis in SCA provides valuable insights into thedisease 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