National Centre for Cell Science, NCCS Complex, Ganeshkhind, SPPU Campus, Pune 411007, India.
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, P.O. Box 11099, Taif 21944, Saudi Arabia.
Molecules. 2022 May 13;27(10):3142. doi: 10.3390/molecules27103142.
In many regions of the world, Leishmaniasis is a cause of substantial mortality and ailment. Due to impediment in available treatment, development of novel and effective treatments is indispensable. Significance of autophagy has been accentuated in infectious disease as well as in Leishmaniasis, and it is having capability to be manifested as a therapeutic target. By evincing autophagy as a novel therapeutic regime, this study emphasized on the critical role of ATG4.1-ATG8 and ATG5-ATG12 complexes in species. The objective here was to identify ATG8 as a potential therapeutic target in . R71T, P56E, R18P are the significant mutations which shows detrimental effect on ATG8 while Arg276, Arg73, Cys75 of ATG4.1 and Val88, Pro89, Glu116, Asn117, and Gly120 are interacting residues of ATG8. Along with this, we also bring into spotlight an enticing role of Thiabendazole derivatives that interferes with the survival mechanisms by targeting ATG8. Further, the study claims that thiabendazole can be a potential drug candidate to target autophagy process in the infectious disease Leishmaniasis.
在世界许多地区,利什曼病是导致大量死亡和疾病的原因。由于现有治疗方法存在障碍,因此开发新型有效治疗方法是必不可少的。自噬在传染病和利什曼病中的重要性已经得到强调,并且它有可能成为一个治疗靶点。通过证明自噬是一种新的治疗方案,本研究强调了 ATG4.1-ATG8 和 ATG5-ATG12 复合物在 物种中的关键作用。本研究的目的是确定 ATG8 作为 的潜在治疗靶点。R71T、P56E、R18P 是对 ATG8 具有不利影响的重要突变,而 ATG4.1 的 Arg276、Arg73 和 Cys75 和 ATG8 的 Val88、Pro89、Glu116、Asn117 和 Gly120 是相互作用残基。除此之外,我们还强调了噻苯达唑衍生物的诱人作用,它通过靶向 ATG8 来干扰生存机制。此外,该研究声称噻苯达唑可以成为针对传染病利什曼病中自噬过程的潜在药物候选物。