作为恶性疟原虫及其人类宿主细胞死亡调节剂的小热休克蛋白

Francisca Magum Timothy, T. Zininga
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摘要

恶性疟原虫是严重疟疾的主要病原体,在其生命周期中,恶性疟原虫在变温蚊子和恒温动物人类体内都能茁壮成长,并能适应具有挑战性的温度变化。要在如此多变的环境中生存,就必须开发出强大的机制,包括复杂的蛋白质折叠系统,以减轻蛋白病。寄生虫需要控制宿主细胞的存活,这将影响其发育和繁殖的机会。热休克蛋白(Hsps)是这一系统的核心,其中小型热休克蛋白(sHsps)在维持蛋白稳态(蛋白质平衡)方面发挥着关键作用。在人类和恶性疟原虫体内,已经发现了大量的 sHsps,这使它们成为诊断和药物开发战略中具有吸引力的候选生物标志物。越来越多的证据表明,这些 sHsps 参与了细胞死亡过程,可能会影响疾病的发病机制。尽管sHsps具有重要意义,但它们在恶性疟原虫适应应激条件过程中的确切功能在很大程度上仍然未知。人类与恶性疟原虫之间的 sHsps 结构比较分析揭示了物种特异性差异。尽管三级结构保持不变,但寄生虫 sHsps 中发现了独特的基序,这些基序可能会调节特殊的伴侣功能。这篇综述讨论了人类宿主和寄生虫中 sHsps 的保守和独特基调,深入探讨了共同和独特的属性。这些发现揭示了针对物种特异性靶向 sHsps 的潜力,sHsps 是细胞死亡过程中的参与者,可促进创新的生物标志物鉴定方法。随着疟疾继续肆虐撒哈拉以南的非洲地区,了解指导寄生虫生存的分子错综复杂的关系对于开发更有效的干预措施来应对这一全球健康危机至关重要。
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Small heat shock proteins as modulators of cell death in Plasmodium falciparum parasites and its human host
Plasmodium falciparum, the predominant cause of severe malaria, thrives within both poikilotherm mosquitoes and homeotherm humans, navigating challenging temperature shifts during its life cycle. Survival in such varying environments necessitate the development of robust mechanisms, including a sophisticated protein folding system to mitigate proteopathy. The parasite needs to control the survival of its host cells which affects its chances of development and propagation. Central to this system are heat shock proteins (Hsps), among which small Hsps (sHsps) play pivotal roles in maintaining proteostasis (protein homeostasis). In both humans and P. falciparum, numerous sHsps have been identified, making them attractive candidates as biomarkers for diagnostic and drug development strategies. Evidence is accumulating suggesting that these sHsps participate in cell death processes, potentially influencing disease pathogenesis. Despite their significance, the precise functions of sHsps in P. falciparum’s adaptation to stress conditions remains largely unknown. Comparative structural analysis of sHsps between human and P. falciparum reveals species-specific variations. Despite conserved tertiary structures, unique motifs are found in parasite sHsps which may modulate specialised chaperone functions. This review discusses the conserved and distinctive motifs of sHsps from the human host and the parasite, offering insights into shared and unique attributes. These findings illuminate the potential for species-specific targeting of sHsps, as players in cell death processes that may foster innovative biomarker identification approaches. As malaria continues to ravage Sub-Saharan Africa, understanding the molecular intricacies guiding parasite survival are essential in the development of interventions with heightened efficacy against this global health crisis.
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