Vascular calcification: High incidence sites, distribution, and detection.

Vascular calcification is an important pathological change in a variety of disease states such as atherosclerosis (AS), diabetes, chronic kidney disease (CKD), hypertension, and is a strong predictor of cardiovascular events. The distribution and location of calcification in different vessels may have different clinical effects and prognosis. Therefore, the study of high-risk sites of vascular calcification will help us to better understand the prevention, diagnosis, and treatment of related diseases, as well as to evaluate the efficacy and prognosis. So far, although there are some studies on the sites with high incidence of vascular calcification, there is a lack of systematic sorting out the distribution and location of vascular calcification in humans. Based on this, relevant databases were searched, literatures were retrieved, analyzed, and summarized, and the locations of high incidence of vascular calcification and their distribution characteristics, the relationship between high incidence of vascular calcification and hemodynamics, and the common detection methods of high incidence of vascular calcification were systematically described, hoping to provide help for clinical and research.

Macrophage polarisation and inflammatory mechanisms in atherosclerosis: Implications for prevention and treatment.

Atherosclerosis is a chronic inflammatory disease characterised by plaque accumulation in the arteries. Macrophages are immune cells that are crucial in the development of atherosclerosis. Macrophages can adopt different phenotypes, with the M1 phenotype promoting inflammation while the M2 phenotype counteracting it. This review focuses on the factors that drive the polarisation of M1 macrophages towards a pro-inflammatory phenotype during AS. Additionally, we explored metabolic reprogramming mechanisms and cytokines secretion by M1 macrophages. Hyperlipidaemia is widely recognised as a major risk factor for atherosclerosis. Modified lipoproteins released in the presence of hyperlipidaemia can trigger the release of cytokines and recruit circulating monocytes, which adhere to the damaged endothelium and differentiate into macrophages. Macrophages engulf lipids, leading to the formation of foam cells. As atherosclerosis progresses, foam cells become the necrotic core within the atherosclerotic plaques, destabilising them and triggering ischaemic disease. Furthermore, we discuss recent research focusing on targeting macrophages or inflammatory pathways for preventive or therapeutic purposes. These include statins, PCSK9 inhibitors, and promising nanotargeted drugs. These new developments hold the potential for the prevention and treatment of atherosclerosis and its related complications.

Effects of Different Carbohydrate Content Diet on Gut Microbiota and Aortic Calcification in Diabetic Mice.

Introduction: Vascular calcification is a major cause of cardiovascular accidents in patients with type 2 diabetes mellitus. This study aimed to investigate the impact of carbohydrates on gut microbiota and aortic calcification in diabetic ApoE-/- mice. Methods: The diabetic ApoE-/- mice were randomly divided into 4 groups: ketogenic diet group, low carbohydrate diet group, medium carbohydrate diet group, and high carbohydrate diet group. The mice were fed continuously for 6 months, with blood glucose, blood ketone and body weight monitored monthly. Lipid metabolism indicators and inflammatory factors were detected using ELISA. The intestinal barrier, atherosclerotic lesion areas, and vascular calcifications were analyzed based on their morphology. Gut microbiota was analyzed using 16S rRNA genes. Results: We found that ketogenic diet played some roles improving glucose, lipid metabolism, and inflammation. Ketogenic diet could improve the intestinal barrier to some extent and increase intestinal bacteria. Compared to the other three groups, the relative abundance of genus Allobaculum, species Blautia producta and Clostridium Ramosum in the ketogenic diet group was significantly increased (P <0.05), which has protective effects in diabetic ApoE-/- mice. Conclusion: Ketogenic diet could delay the onset of aortic atherosclerosis, aortic calcification and improve intestinal barrier function in diabetic ApoE-/- mice.

USP10 alleviates Nε-carboxymethyl-lysine-induced vascular calcification and atherogenesis in diabetes mellitus by promoting AMPK activation.

Vascular calcification (VC) is a characteristic feature in patients with diabetes mellitus (DM) and is closely associated with the osteogenic differentiation of vascular smooth muscle cells (VSMCs). Ubiquitin-Specific Protease 10 (USP10) has been shown to regulate multiple cellular processes; however, its relationship with diabetic VC remains unclear. This study aims to elucidate the role of USP10 in VC development and the underlying regulatory mechanisms. Nε-carboxymethyl lysine (CML) was significantly increased in calcified ateries from diabetic atherosclerosis ApoE-/- mice fed with high-fat diets. CML downregulated USP10 expression in VSMCs and calcified mice coronary arteries, as assessd by Western blotting, RT-qPCR,immunofluorescence and immunohistochemistry. Loss-and gain-of-function experiments were conducted both in vitro and in vivo to verify the biological functions of USP10. Ectopic expression of USP10 mitigated the severity of VC. With regard to the mechanism, the interaction between USP10 and AMPKα was investigated through double-label immunofluorescence and Co-immunoprecipitation. In vitro ubiquitination assay revealed that USP10 was capable of mediating AMPKα ubiquitination and caused increased AMPKα phosphorylation level at Thr172. Moreover, the anticalcification effect of USP10 was reversed by pharmacological inhibition of AMPK signaling pathway. The current fundings suggest an important role of USP10 in diabetic VC progression, at least in part, via mediating the ubiquitination and activation of AMPKα. USP10 may serve as a novel therapeutic target for the treatment of diabetic VC.

Protective Effect of CD137 Deficiency against Post-infarction Cardiac Fibrosis and Adverse Cardiac Remodeling via ERK1/2 Signaling Pathways.

Myocardial fibrosis, a common complication of myocardial infarction (MI), is characterized by excessive collagen deposition and can result in impaired cardiac function. The specific role of CD137 in the development of post-MI myocardial fibrosis remains unclear. Thus, this study aimed to elucidate the effects of CD137 signaling using CD137 knockout mice and in vitro experiments. CD137 expression levels progressively increased in the heart following MI, particularly in myofibroblast, which play a key role in fibrosis. Remarkably, CD137 knockout mice exhibited improved cardiac function and reduced fibrosis compared to wild-type mice at day 28 post-MI. The use of Masson's trichrome and picrosirius red staining demonstrated a reduction in the infarct area and collagen volume fraction in CD137 knockout mice. Furthermore, the expression of alpha-smooth muscle actin (α-SMA) and collagen I, key markers of fibrosis, was decreased in heart tissues lacking CD137. In vitro experiments supported these findings, as CD137 depletion attenuated cardiac fibroblast differentiation, and migration, and collagen I synthesis. Additionally, the administration of CD137L recombinant protein further promoted α-SMA expression and collagen I synthesis, suggesting a pro-fibrotic effect. Notably, the application of an inhibitor targeting the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway attenuated the pro-fibrotic effects of CD137L. To conclude, this study provides evidence that CD137 plays a significant role in promoting myocardial fibrosis after MI. Inhibition of CD137 signaling pathways may hold therapeutic potential for mitigating pathological cardiac remodeling and improving post-MI cardiac function.

Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.

Presently, the mechanism of occurrence and development of vascular calcification (VC) is not fully understood; a range of evidence suggests a positive association between diabetes mellitus (DM) and VC. Furthermore, the increasing burden of central vascular disease in patients with chronic kidney disease (CKD) may be due, at least in part, to VC. In this review, we will review recent advances in the mechanisms of VC in the context of CKD and diabetes. The study further unveiled that VC is induced through the stimulation of pro-inflammatory factors, which in turn impairs endothelial function and triggers similar mechanisms in both disease contexts. Notably, hyperglycemia was identified as the distinctive mechanism driving calcification in DM. Conversely, in CKD, calcification is facilitated by mechanisms including mineral metabolism imbalance and the presence of uremic toxins. Additionally, we underscore the significance of investigating vascular alterations and newly identified molecular pathways as potential avenues for therapeutic intervention.

Therapeutic Strategies for Angiogenesis Based on Endothelial Cell Epigenetics.

With the in-depth investigation of various diseases, angiogenesis has gained increasing attention. Among the contributing factors to angiogenesis research, endothelial epigenetics has emerged as an influential player. Endothelial epigenetic therapy exerts its regulatory effects on endothelial cells by controlling gene expression, RNA, and histone modification within these cells, which subsequently promotes or inhibits angiogenesis. As a result, this therapeutic approach offers potential strategies for disease treatment. The purpose of this review is to outline the pertinent mechanisms of endothelial cell epigenetics, encompassing glycolysis, lactation, amino acid metabolism, non-coding RNA, DNA methylation, histone modification, and their connections to specific diseases and clinical applications. We firmly believe that endothelial cell epigenetics has the potential to become an integral component of precision medicine therapy, unveiling novel therapeutic targets and providing new directions and opportunities for disease treatment.

Acetylated Histone Modifications: Intersection of Diabetes and Atherosclerosis.

ABSTRACT: Worldwide, type 2 diabetes is predominant form of diabetes, and it is mainly affected by the environment. Furthermore, the offspring of patients with type 2 diabetes and metabolic disorder syndrome may have a higher risk of diabetes and cardiovascular disease, which indicates that the environmental impact on diabetes prevalence can be transmitted across generations. In the process of diabetes onset and intergenerational transmission, the genetic structure of the individual is not directly changed but is regulated by epigenetics. In this process, genes or histones are modified, resulting in selective expression of proteins. This modification will affect not only the onset of diabetes but also the related onset of atherosclerosis. Acetylation and deacetylation may be important regulatory factors for the above lesions. Therefore, in this review, based on the whole process of atherosclerosis evolution, we explored the possible existence of acetylation/deacetylation caused by diabetes. However, because of the lack of atherosclerosis-related acetylation studies directly based on diabetic models, we also used a small number of experiments involving nondiabetic models of related molecular mechanisms.

Endothelial-to-mesenchymal transition: New insights into vascular calcification.

With the continuous progress of atherosclerosis research, the significant pathological change of it--vascular calcification (VC), gains increasing attention. In recent years, numerous studies have demonstrated that it is an independent predictor of death risk of cardiovascular disease, and it has a strong correlation with poor clinical prognosis. As the world's population continues to age, the occurrence of VC is expected to reach its highest point in the near future. Therefore, it is essential to investigate ways to prevent or even reverse this process for clinical purposes. Endothelial-to-mesenchymal transition (EndMT) describes the progressive differentiation of endothelial cells into mesenchymal stem cells (MSCs) under various stimuli and acquisition of pluripotent cell characteristics. More and more studies show that EndMT plays a vital role in various cardiovascular diseases, including atherosclerosis, vascular calcification and heart valvular disease. EndMT is also involved in the formation and progression of VC. This review vividly describes the history, characteristics of EndMT and how it affects the endothelial cell process, then focuses on the relationship between vascular endothelium, EndMT, amino acid metabolism, and vascular calcification. Finally, it overviews the signal pathway of EndMT and drugs targeting EndMT, hoping to provide new ideas and a theoretical basis for studying potential therapeutic targets of VC.

SIRT3-and FAK-mediated acetylation-phosphorylation crosstalk of NFATc1 regulates Nε-carboxymethyl-lysine-induced vascular calcification in diabetes mellitus.

BACKGROUND AND AIMS: Arterial calcification is the predictor of cardiovascular risk in diabetic patients. Nε-carboxymethyl-lysine (CML), a toxic metabolite, is associated with accelerated vascular calcification in diabetes mellitus (DM). However, the mechanism remains elusive. This study aims to explore the key regulators involved in CML-induced vascular calcification in DM. METHODS: We used Western blot and immuno-staining to test the expression and localization of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) in human samples, a diabetic apolipoprotein E-deficient (ApoE-/-) mouse model, and a vascular smooth muscle cells (VSMC) model. Further, we confirmed the regulator of NFATc1 phosphorylation and acetylation induced by CML. The role of NFATc1 in VSMCs calcification and osteogenic differentiation was explored in vivo and in vitro. RESULTS: In diabetic patients, CML and NFATc1 levels increased in the severe calcified anterior tibial arteries. CML significantly promoted NFATc1 expression and nuclear translocation in VSMCs and mouse aorta. Knockdown of NFATc1 significantly inhibited CML-induced calcification. CML promoted NFATc1 acetylation at K549 by downregulating sirtuin 3 (SIRT3), which antagonized the focal adhesion kinase (FAK) induced NFATc1 phosphorylation at the Y270 site. FAK and SIRT3 affected the nuclear translocation of NFATc1 by regulating the acetylation-phosphorylation crosstalk. NFATc1 dephosphorylation mutant Y270F and deacetylation mutant K549R had opposite effects on VSMC calcification. SIRT3 overexpression and FAK inhibitor could reverse CML-promoted VSMC calcification. CONCLUSIONS: CML enhances vascular calcification in DM through NFATc1. In this process, CML increases NFATc1 acetylation by downregulating SIRT3 to antagonize FAK-induced NFATc1 phosphorylation.

CD137 signaling aggravates myocardial ischemia-reperfusion injury by inhibiting mitophagy mediated NLRP3 inflammasome activation.

BACKGROUND: The inflammatory response caused by the NLRP3 is closely related to the formation of myocardial ischemia-reperfusion injury. Costimulatory receptor CD137 and its ligand play a crucial role in regulating the inflammatory immune response in atherosclerosis, which is the fundamental cause of cardiovascular diseases. However, the roles of CD137 signaling in the process of myocardial ischaemia-reperfusion (IR) injury remain unknown. METHODS: Genetic ablation was used to determine the functional significance of CD137 in myocardial IR injury. Expression of CD137 was examined by Western-blot, quantitative real-time polymerase chain reaction, and immunohistochemistry in a murine IR model by coronary artery ligation. Even's blue-TTC staining and echocardiography to evaluate the severity of myocardial IR injury. Furthermore, HL-1 cardiomyocytes treated with agonist-CD137 recombinant protein were used to explore the underlying mechanism in CD137 signaling-induced NLRP3 inflammasome activation in response to hypoxia/reoxygenation or LPS/ATP. RESULTS: We demonstrated that CD137 knockout significantly improved cardiac function, accompanied by a markedly reduced NLRP3-mediated inflammatory response and IA/AAR which were reversed by mitophagy inhibitor Mdivi-1. Activating CD137 signaling significantly inhibited mitophagy and provoked NLRP3-mediated inflammatory response in H/R-injured or LPS-primed and ATP-stimulated HL-1 cardiomyocytes, the effects of which could be abolished by either anti-CD137 or mitophagy activator FCCP. Besides, mitochondrial ROS was augmented by activating CD137 signaling through the suppression of mitophagy. CONCLUSIONS: Our results reveal that activating CD137 signaling aggravates myocardial IR injury by upregulating NLRP3 inflammasome activation via suppressing mitophagy and promoting mtROS generation.

Nε-(carboxymethyl)lysine promotes lipid uptake of macrophage via cluster of differentiation 36 and receptor for advanced glycation end products.

BACKGROUND: Advanced glycation end products (AGEs) are diabetic metabolic toxic products that cannot be ignored. Nε-(carboxymethyl)lysine (CML), a component of AGEs, could increase macrophage lipid uptake, promote foam cell formation, and thereby accelerate atherosclerosis. The receptor for AGEs (RAGE) and cluster of differentiation 36 (CD36) were the receptors of CML. However, it is still unknown whether RAGE and CD36 play key roles in CML-promoted lipid uptake. AIM: Our study aimed to explore the role of RAGE and CD36 in CML-induced mac-rophage lipid uptake. METHODS: In this study, we examined the effect of CML on lipid uptake by Raw264.7 macrophages. After adding 10 mmol/L CML, the lipid accumulation in macro-phages was confirmed by oil red O staining. Expression changes of CD36 and RAGE were detected with immunoblotting and quantitative real-time polymerase chain reaction. The interaction between CML with CD36 and RAGE was verified by immunoprecipitation. We synthesized a novel N-succinimidyl-4-18F-fluorobenzoate-CML radioactive probe. Radioactive receptor-ligand binding assays were performed to test the binding affinity between CML with CD36 and RAGE. The effects of blocking CD36 or RAGE on CML-promoting lipid uptake were also detected. RESULTS: The study revealed that CML significantly promoted lipid uptake by macro-phages. Immunoprecipitation and radioactive receptor-ligand binding assays indicated that CML could specifically bind to both CD36 and RAGE. CML had a higher affinity for CD36 than RAGE. ARG82, ASN71, and THR70 were the potential interacting amino acids that CD36 binds to CML Anti-CD36 and anti-RAGE could block the uptake of CML by macrophages. The lipid uptake promotion effect of CML was significantly attenuated after blocking CD36 or RAGE. CONCLUSION: Our results suggest that the binding of CML with CD36 and RAGE promotes macrophage lipid uptake.

Role of galectin-3 in vascular calcification.

Vascular calcification is an abnormal process in which bone specific hydroxyapatite crystals are actively deposited on the vascular wall mediated by phenotypic differentiated smooth muscle cells and other mesenchymal cells under various pathological conditions. It is one of the important characteristics in the occurrence and development of atherosclerosis, prevalent in patients with type 2 diabetes and advanced chronic kidney disease, especially those requiring maintenance hemodialysis, with severely threatening human health. Previous studies have shown that the early diagnosis and control of vascular calcification is of great significance for cardiovascular risk stratification, prevention of acute cardiovascular events, which can greatly improve the prognosis and quality of life of patients. Galectins are a family of lectin superfamily. It is widely distributed in various animals and plays an important role in many physiological and pathological processes, such as cell adhesion, apoptosis, inflammatory response, tumor metastasis and so on. Many biomarker-and association-related studies and Preclinical-mechanistic studies have suggested that galactose-specific lectin-3 (galectin-3) plays an important role in vascular calcification and vascular intimal calcification (VIC) calcification induced by Wnt/ßcatenin signaling pathway, NF-κB signaling pathway and ERK1/2 signaling pathway. This paper mainly expounds the role and mechanism of galectin-3 in vascular calcification under different pathological conditions including atherosclerosis, diabetes and chronic kidney disease.

Role of ceramides in diabetic foot ulcers (Review).

Diabetes mellitus (DM) is a metabolic disorder, which if not managed properly, can lead to serious health problems over time and impose significant financial burden on the patient, their family and society as a whole. The study of this disease and the underlying biological mechanism is gaining momentum. Multiple pieces of conclusive evidence show that ceramides are involved in the occurrence and development of diabetes. The present review focuses on the function of ceramides, a type of sphingolipid signaling molecule, to provide a brief description of ceramides and their metabolism, discuss the significant roles of ceramides in the healthy skin barrier, and speculate on the potential involvement of ceramides in the pathogenesis and development of diabetic foot ulcers (DFUs). Understanding these aspects of this disease more thoroughly is crucial to establish how ceramides contribute to the etiology of diabetic foot infections and identify possible therapeutic targets for the treatment of DFUs.

Disruption of COMMD1 accelerates diabetic atherosclerosis by promoting glycolysis.

AIMS: Diabetes will lead to serious complications, of which atherosclerosis is the most dangerous. This study aimed to explore the mechanisms of diabetic atherosclerosis. METHODS: ApoE-/- mice were fed with an high-fat diet diet and injected with streptozotocin to establish an in vivo diabetic atherosclerotic model. RAW 264.7 cells were treated with oxidized low-density lipoprotein particles (ox-LDL) and high glucose to produce an in vitro diabetic atherosclerotic model. RESULTS: In this study, we showed that diabetes promoted the progression of atherosclerosis in ApoE-/- mice and that high glucose potentiates macrophage proinflammatory activation and foam cell formation. Mechanistically, Copper metabolism MURR1 domain-containing 1(COMMD1) deficiency increased proinflammatory activation and foam cell formation, characterized by increased glycolysis, and then accelerated the process of atherosclerosis. Furthermore, 2-Deoxy-D-glucose (2-DG) reversed this effect. CONCLUSION: Taken together, we provided evidence that the lack of COMMD1 accelerates diabetic atherosclerosis via mediating the metabolic reprogramming of macrophages. Our study provides evidence of a protective role for COMMD1 and establishes COMMD1 as a potential therapeutic strategy in patients with diabetic atherosclerosis.

Role and progress of artificial intelligence in radiodiagnosing vascular calcification: a narrative review.

Background and Objective: Vascular calcification has important clinical significance due to its vital prognostic value for cardiovascular diseases, chronic kidney disease (CKD), diabetes, fracture, and other multisystem diseases. Radiology is the main diagnostic method of it, but facing great pressure such as the increasing workload and decreasing working accuracy rate. Therefore, radiology needs to find a way out to better realize the clinical value of vascular calcification. Artificial intelligence (AI) encompasses any algorithm imitating human intelligence. AI has shown great potential in image analysis, such as its high speed and accuracy, becoming the savior of the current situation. In order to promote more rational utilization, the role and progress of AI in this field were reviewed. Methods: A search was conducted in PubMed and Web of Science. The key words included "artificial intelligence", "machine learning", "deep learning", and "vascular calcification". The qualitative analysis of literature was achieved through repeated deliberation after refining valuable content. The theme is the role and progress of AI in the diagnostic radiology of vascular calcification. Key Content and Findings: Sixty-two articles were included. AI has been applied to the diagnostic radiology of 5 types of vascular calcification, including coronary artery calcification (CAC), thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and breast artery calcification (BAC). Deep learning (DL), the latest technology in this field has been well applied and satisfactorily performed. Radiologists have been able to achieve efficient diagnosis of 5 types of vascular calcification through AI, with reliable accuracy. Conclusions: Increasingly, advanced AI has achieved an accuracy comparable to that of human experts, with a faster speed. Moreover, the ability to reduce noise and artifacts enables more imaging equipment to obtain reliable quantification. AI has acquired the ability to cooperate with radiology departments in future work. However, the research in AAC and carotid artery calcification can be more in-depth, and more types of vascular calcification and more fields of radiology should be expanded to. The interpretation of results made by AI and the promotion of existing achievements to the development of other disciplines are also the focus in future.

Advances in Glycolysis Metabolism of Atherosclerosis.

Glycolysis is an important way for various cells such as vascular wall endothelial cells, smooth muscle cells, macrophages, and other cells to obtain energy. In pathological conditions, it can participate in the process of AS by regulating lipid deposition, calcification, angiogenesis in plaques, etc., together with its metabolite lactic acid. Recent studies have shown that lactate-related lactylation modifications are ubiquitous in the human proteome and are involved in the regulation of various inflammatory diseases. Combined with the distribution and metabolic characteristics of cells in the plaque in the process of AS, glycolysis-lactate-lactylation modification may be a new entry point for targeted intervention in atherosclerosis in the future. Therefore, this article intends to elaborate on the role and mechanism of glycolysis-lactate-lactylation modification in AS, as well as the opportunities and challenges in targeted therapy, hoping to bring some help to relevant scholars in this field. In atherosclerosis, glycolysis, lactate, and lactylation modification as a metabolic sequence affect the functions of macrophages, smooth muscle cells, endothelial cells, lymphocytes, and other cells and interfere with processes such as vascular calcification and intraplaque neovascularization to influence the progression of atherosclerosis.

Nε-Carboxymethyl-Lysine Mediates Vascular Calcification in Diabetes Caused by Impaired Osteoclastic Resorption Activity Through NFATc1-GNPTAB.

Nε-carboxymethyl-lysine (CML) is closely associated with vascular calcification in diabetes. Osteoclasts are the only cells with bone resorption activity that have the potential to reverse calcification. This study aimed to investigate the mechanism of CML in the bone resorption activity of macrophage-derived osteoclasts in diabetic calcified plaques. Macrophage-derived osteoclasts were found to be present in calcified plaques of the anterior tibial artery in patients with diabetic amputation. Furthermore, in vitro studies showed that CML induced the differentiation of macrophages into osteoclasts, although, the bone resorption activity of these macrophage-derived osteoclasts was impaired. CML significantly increased the levels of NFATc1and GNPTAB. In vivo studies showed that there was more calcium deposition and less TRAP was less in the CML group while this effect was reversed after silencing of NFATc1. In conclusion, CML mediates NFATc1-GNPTAB to regulate bone resorption activity of osteoclasts in diabetic calcified plaques. CML promotes macrophage differentiation into osteoclasts, but their function is impaired in diabetic calcified plaques through NFATc1-GNPTAB, which eventually leads to the further progression of vascular calcification in diabetes.

Diabetic Retinopathy and Cardiovascular Disease: A Literature Review.

Diabetic complications can be divided into macrovascular complications such as cardiovascular disease and cerebrovascular disease and microvascular complications such as diabetic retinopathy, diabetic nephropathy and diabetic neuropathy. Among them, cardiovascular disease (CVD) is an important cause of death in diabetic patients. Diabetes retinopathy (DR) is one of the main reasons for the increasing disability rate of diabetes. In recent years, some studies have found that because DR and CVD have a common pathophysiological basis, the occurrence of DR and CVD are inseparable, and to a certain extent, DR can predict the occurrence of CVD. With the development of technology, the fundus parameters of DR can be quantitatively analyzed as an independent risk factor of CVD. In addition, the cytokines related to DR can also be used for early screening of DR. Although many advances have been made in the treatment of CVD, its situation of prevention and treatment is still not optimistic. This review hopes to discuss the feasibility of DR in predicting CVD from the common pathophysiological mechanism of DR and CVD, the new progress of diagnostic techniques for DR, and the biomarkers for early screening of DR.