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疟原虫青蒿素耐药性的多种途径。

The many paths to artemisinin resistance in Plasmodium falciparum.

机构信息

Department of Biology, Indian Institute of Science Education and Research, Pune, India.

Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, India.

出版信息

Trends Parasitol. 2023 Dec;39(12):1060-1073. doi: 10.1016/j.pt.2023.09.011. Epub 2023 Oct 11.

Abstract

Emerging resistance against artemisinin (ART) poses a major challenge in controlling malaria. Parasites with mutations in PfKelch13, the major marker for ART resistance, are known to reduce hemoglobin endocytosis, induce unfolded protein response (UPR), elevate phosphatidylinositol-3-phosphate (PI3P) levels, and stimulate autophagy. Nonetheless, PfKelch13-independent resistance is also reported, indicating extensive complementation by reconfiguration in the parasite metabolome and transcriptome. These findings implicate that there may not be a single 'universal identifier' of ART resistance. This review sheds light on the molecular, transcriptional, and metabolic pathways associated with ART resistance, while also highlighting the interplay between cellular heterogeneity, environmental stress, and ART sensitivity.

摘要

青蒿素(ART)耐药性的出现对疟疾的控制构成了重大挑战。已知具有 PfKelch13 突变的寄生虫可减少血红蛋白内吞作用、诱导未折叠蛋白反应 (UPR)、提高磷脂酰肌醇-3-磷酸 (PI3P) 水平并刺激自噬。尽管如此,也有报道称存在 PfKelch13 非依赖性耐药性,这表明寄生虫代谢组和转录组的重新配置可进行广泛的代偿。这些发现表明,ART 耐药性可能没有单一的“通用标识符”。本综述阐明了与 ART 耐药性相关的分子、转录和代谢途径,同时强调了细胞异质性、环境压力和 ART 敏感性之间的相互作用。

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