The pathogenesis of retinopathy in highly myopic eyes is of two kinds: – the biological theory, that is, the role of genetic factors, and the mechanical theory, that is, the weakness of the posterior spherical wall and the occurrence of myopia and its fundus lesions on the elongated surface. Although the exact etiology and pathogenesis are not very clear, the progressive prolongation of the eye axis and the expansion of the posterior spherical segment with degenerative changes as the distinguishing features of high myopia. I. High myopia fundus lesions are closely related to the prolongation of the eye axis. Logically, various causes of progressive lengthening of the eye, posterior spherical expansion and deformation can seriously affect the choroidal microcirculation and make the choroidal vessels straighten and harden, and then pathological changes such as vitreous membrane rupture, pigment epithelial degeneration and atrophy, subretinal neovascularization and hemorrhage occur, and clinically, retinal choroidal atrophy, lacquer crackle-like changes, the Fuch’s spots and other fundus manifestations. Second, the prolongation of the eye axis is associated with a variety of lesions in the fundus, but mainly affects the posterior pole. As the length of the eye axis increases, the number of lesions in the posterior pole and diffuse lesions, including posterior pole lesions, increases. The fundus lesions in high myopia are a diverse and complex body of degenerative lesions, and their pathological features go far beyond the scope of refractive error and are difficult to explain by one theory. For example, the mechanistic theory suggests that fundus lesions are the result of excessive elongation of the eye axis, which is due to abnormal expansion of the scleral structure and relatively high intraocular pressure, so it seems that the elongation of the eye axis is not the initial cause of high myopia. Moreover, mechanical dilatation of the posterior segment of the globe can be the cause of the formation of pars plana choroidal atrophy spots, posterior scleral staphyloma, etc., but it does not account for the entire formation mechanism of the intricate high myopia fundus lesions. For example, lacrimal-like changes involve pathological changes in the choroidal vessels, Fuch’s membrane, and pigment epithelium, while the formation of Fuch’s spots is associated with subretinal neovascularization, hemorrhage, mechanization, and pigment proliferation. These lesions are notable for involving alterations in the microcirculation of the fundus. For example, Yang-Gui Yu found that subretinal neovascularization in high myopia occurs mostly in myopia from C11D to C25D, and in myopia above C25D, neovascularization is not seen due to large atrophy in the posterior pole of the fundus. As to in what way and by what mechanism genetic factors actually play a role in the formation and development of high myopia, it remains unclear. In conclusion, excessive prolongation of the eye axis is a risk factor and intermediate link in the formation and development of high myopia fundus lesions, but it is not the starting cause. The purpose of analyzing and exploring the intrinsic connection and interaction between eye axis length and fundus lesions is to seek control of eye axis prolongation. We aim to find effective methods to alleviate fundus lesions and achieve the ultimate goal of preventing and treating high myopia.