Diabetic microangiopathy is the common pathological basis for many serious vascular complications of diabetes such as diabetic nephropathy (DN), diabetic retinopathy, diabetic cardiomyopathy, and diabetic wet gangrene. Microcirculatory disorders, microangiomas and microvascular basement membrane thickening are typical lesions of diabetic microangiopathy. The exact pathogenesis of diabetic microangiopathy has not been fully elucidated by modern medicine, but the following important hypotheses have been developed. (1) Hemodynamic abnormalities: Hemodynamic changes are important initiating factors of microangiopathy. Hyperglycemia-induced renal perfusion and hyperfiltration is an important mechanism for the occurrence of diabetic microvascular complications of DN, and hyperglycemia can inhibit tubular? s feedback, promoting the release of vasodilator substances prostaglandin and cardiac natriuretic hormone and increased NO secretion, causing the expansion of small glomerular inlet arteries and the increase of intra-glomerular pressure, resulting in glomerular hyperfiltration. (2) Protein non-enzymatic glycosylation theory: It is believed that in a hyperglycemic environment, various tissue proteins can undergo non-enzymatic glycosylation reactions, and glucose chemically combines with proteins at the early stage of glycosylation to form reversible early glycosylation products, which then undergo rearrangement, cross-linking, and finally form glycation end products (AGE). The result is increased permeability of microvessels, thickening of basement membrane, stagnation of blood flow, and even occlusion of microvessels, resulting in diabetic microangiopathy. (3) Polyol channel activity increase theory: polyol channel activity is composed of a series of enzyme systems, the most important one is aldose reductase, polyol channel activity increases when hyperglycemia, aldose reductase activity increases, the process of glucose conversion into sorbitol catalyzed by aldose reductase increases, a large amount of sorbitol accumulates in tissue cells, and becomes one of the main mechanisms of chronic complications of diabetes. (4) Tissue oxidation and glycosylation theory: It is believed that there are extensive protein non-enzymatic glycosylation and oxidative modification reactions in diabetic patients, and the two promote each other, as a result, lipid oxidation, superoxide radicals and non-enzymatic glycosylation together cause damage to tissues, resulting in pathological changes such as increased microvascular permeability and thickening of microvascular basement membrane. (5) Involvement of angiotensin II (ATII) and cell growth factors, with the progress of molecular biology research in recent years, it has been confirmed that ATII and various cytokines such as interleukin-6 (IL-6), tumor necrosis factor (TNF) and transforming growth factor (TGF-β) are involved in the occurrence and development of diabetic nephropathy, a microvascular complication of diabetes mellitus. The expression of TGF-β increases the expression of type IV collagen messenger ribonucleic acid (mRNA) and stimulates glomerular thylakoid cells to synthesize and secrete collagen IV. TNF promotes the proliferation of thylakoid cells and the secretion of extracellular matrix. (6) Hyperlipidemia: recent studies have shown that disorders of lipid metabolism can induce platelet accumulation and release through the production of oxygen free radicals, induce monocyte? Macrophage infiltration and release of a variety of hydrolases and cytokines, interference with prostaglandin synthesis and other multifaceted mechanisms involved in the pathological process of diabetic microangiopathy. (7) Microcirculatory disorders: A large number of studies have confirmed the prevalence of microcirculatory disorders in patients with diabetic microangiopathy, mainly manifested by changes in microvascular morphology, microbleeding disorders, and changes in the physicochemical properties of blood showing hypercoagulation, hyperaggregation, hyperintensity and hyperviscosity, which become important mechanisms for the formation of diabetic microangiopathy. The above theories have certain theoretical and experimental bases, but none of them can fully elucidate the pathogenesis of diabetic microangiopathy, therefore, it is especially important to strengthen the basic research on the pathogenesis of diabetic microangiopathy.