Implicating extracellular vesicles in Plasmodium falciparum artemisinin resistance development.

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2021-06-01 Epub Date: 2021-04-24 DOI:10.1111/tra.12787

Kwesi Z Tandoh, Michael D Wilson, Neils B Quashie, Nancy O Duah-Quashie

引用次数: 5

Abstract

Plasmodium falciparum malaria remains a disease of significant public health impact today. With the risk of emerging artemisinin resistance stalling malaria control efforts, the need to deepen our understanding of the parasite's biology is dire. Extracellular vesicles (EVs) are vital to the biology of P. falciparum and play a role in the pathogenesis of malaria. Recent studies have also shown that EVs may play a role in the development of artemisinin resistance in P. falciparum. Here, we highlight evidence on EVs in P. falciparum biology and malaria pathogenesis and argue that there is sufficient ground to propose a role for EVs in the development of P. falciparum artemisinin resistance. We suggest that EVs are actively secreted functional organelles that contribute to cellular homeostasis in P. falciparum-infected red blood cells under artemisinin pressure. Further exploration of this hypothesized EVs-based molecular mechanism of artemisinin resistance will aid the discovery of novel antimalarial therapies.

查看原文本刊更多论文

恶性疟原虫的细胞外囊泡与青蒿素耐药性的关系。

恶性疟原虫疟疾今天仍然是一种对公共卫生产生重大影响的疾病。由于出现青蒿素耐药性的风险阻碍了疟疾控制工作，我们迫切需要加深对这种寄生虫生物学的理解。细胞外囊泡(EVs)对恶性疟原虫的生物学至关重要，并在疟疾的发病机制中发挥作用。最近的研究还表明，EVs可能在恶性疟原虫产生青蒿素耐药性的过程中发挥作用。在此，我们强调了EVs在恶性疟原虫生物学和疟疾发病机制中的证据，并认为有足够的理由提出EVs在恶性疟原虫青蒿素耐药性发展中的作用。我们认为，在青蒿素压力下，EVs是恶性疟原虫感染红细胞中积极分泌的功能细胞器，有助于细胞稳态。进一步探索这种假设的基于ev的青蒿素耐药分子机制将有助于发现新的抗疟疾疗法。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.