The search for host factors that leads to malaria parasite synchronization has been the focus of several laboratories. The host hormone melatonin synchronizes Plasmodium falciparum in culture by increasing the number of mature parasite stages through a PLC-IP3 activation. Melatonin signaling is linked to crosstalk between Ca²⁺-cAMP that results in PKA activation. Two other kinases, PfPK7 and PfeIK1, and the nuclear protein PfMORC that lacks melatonin sensitivity in the inducible knock-down parasites are also identified as part of the hormone-signal transduction pathways. Melatonin also modulates P. falciparum mitochondrial fission genes FIS1, DYN1, and DYN2 in a stage-specific manner. How these multiple molecular mechanisms are orchestrated to lead to parasite synchronization is a fascinating and opened biological question.

寻找导致疟疾寄生虫同步的宿主因素一直是几个实验室的重点。宿主激素褪黑激素通过 PLC-IP3 激活增加成熟寄生虫阶段的数量，从而同步培养物中的恶性疟原虫。褪黑激素信号与导致 PKA 激活的Ca ²⁺ -cAMP之间的串扰有关。另外两种激酶 PfPK7 和 PfeIK1 以及在诱导型敲低寄生虫中缺乏褪黑激素敏感性的核蛋白 PfMORC 也被确定为激素信号转导途径的一部分。褪黑激素也调节恶性疟原虫线粒体裂变基因 FIS1、DYN1 和 DYN2 以特定阶段的方式。如何协调这些多重分子机制以导致寄生虫同步是一个引人入胜且开放的生物学问题。