Glucosyltransferases (Gtfs) play critical roles in the etiology and pathogenesis of Streptococcus mutans (S. mutans)- mediated dental caries including early childhood caries. Gtfs enhance the biofilm formation and promotes colonization of cariogenic bacteria by generating biofilm extracellular polysaccharides (EPSs), the key virulence property in the cariogenic process. Therefore, Gtfs have become an appealing target for effective therapeutic interventions that inhibit cariogenic biofilms. Importantly, targeting Gtfs selectively impairs the S. mutans virulence without affecting S. mutans existence or the existence of other species in the oral cavity. Over the past decade, numerous Gtfs inhibitory molecules have been identified, mainly including natural and synthetic compounds and their derivatives, antibodies, and metal ions. These therapeutic agents exert their inhibitory role in inhibiting the expression gtf genes and the activities and secretion of Gtfs enzymes with a wide range of sensitivity and effectiveness. Understanding molecular mechanisms of inhibiting Gtfs will contribute to instructing drug combination strategies, which is more effective for inhibiting Gtfs than one drug or class of drugs. This review highlights our current understanding of Gtfs activities and their potential utility, and discusses challenges and opportunities for future exploration of Gtfs as a therapeutic target.

葡萄糖基转移酶（Gtfs）在变形链球菌（S. mutans）介导的龋齿（包括儿童早期龋齿）的病因和发病机制中发挥着关键作用。 GTfs 通过产生生物膜胞外多糖 (EPS) 来增强生物膜形成并促进致龋细菌定植，EPS 是致龋过程中的关键毒力特性。因此，Gtfs 已成为抑制致龋生物膜的有效治疗干预措施的一个有吸引力的目标。重要的是，靶向Gtfs选择性地削弱变形链球菌的毒力，而不影响口腔中变形链球菌的存在或其他物种的存在。在过去的十年中，已经鉴定出许多Gtfs抑制分子，主要包括天然和合成的化合物及其衍生物、抗体和金属离子。这些治疗剂发挥其抑制作用，抑制gtf基因的表达以及Gtfs酶的活性和分泌，具有广泛的敏感性和有效性。了解抑制 Gtfs 的分子机制将有助于指导药物组合策略，这比一种药物或一类药物更有效地抑制 Gtfs。这篇综述强调了我们目前对 Gtfs 活动及其潜在效用的理解，并讨论了未来探索 Gtfs 作为治疗靶点的挑战和机遇。