越来越多研究证明细胞自噬在骨不连发病、治疗机制中的重要作用。LAP作为新兴的、Rubicon调控的非典型自噬途径，也在维持机体稳态中发挥着巨大作用。由于LAP和典型自噬相互重叠、互补、竞争，必须重新审视骨科与自噬相关的机制研究，确定发病核心机制是典型自噬还是LAP。淫羊藿苷可以通过调节自噬促进成骨、抑制破骨来治疗骨不连，这也是本课题组的研究重点。综合前期研究、查阅资料发现，Ca2+是两条自噬途径的公共上游信号；Rubicon是LAP必需，但抑制典型自噬；Ca2+-CaM/CaMKⅡ、Rubicon都与骨疾病发病机制相关，因此提出“淫羊藿苷→Ca2+-CaM/CaMKⅡ（LAP中）→Rubicon→LAP→自噬→破骨/成骨细胞”假说，通过检测淫羊藿苷干预前后Ca2+流向、流量以及LAP、典型自噬、骨生化标志物等研究其中机制，为诊治骨不连提供新思路。

More and more studies have proved that autophagy plays an essential role in the pathogenesis and treatment mechanism of nonunion. LAP, as a newly emerging, Rubicon-regulated atypical autophagy pathway, also plays an important role in maintaining the body's homeostasis. Since LAP and typical autophagy overlap, complement and compete with each other, it is necessary to re-examine the mechanisms related to autophagy in orthopedics to determine whether the core pathogenesis is typical autophagy or LAP. Icariin can treat nonunion by regulating autophagy to promote osteogenesis and inhibiting osteoclasts, which is also the focus of our research team. Based on previous studies and data, Ca2+ is the common upstream signal of two autophagy pathways. Rubicon is necessary for LAP but inhibits typical autophagy. Ca2+-CAM/CAMKⅡ and Rubicon are all related to the pathogenesis of bone diseases, so the hypothesis of " icariin → Ca2+-CAM/CAMKⅡ (in LAP) →Rubicon→LAP→ typical autophagy → osteoclast/osteoblast" is put forward, which provides new ideas for the diagnosis and treatment of nonunion by detecting Ca2+ direction, flow rate, LAP, typical autophagy and biochemical markers of bone before and after icariin intervention.