209 results about "Myocyte" patented technology

The invention provides a method for producing cell culture meat through 3D scaffold-free co-culture of pseudosciaena crocea stem cell spheres, and belongs to the technical field of preparation of cell culture meat. A method for producing cell culture meat by 3D scaffold-free co-culture of pseudosciaena crocea stem cell spheres comprises the following steps: mixing and inoculating pseudosciaena crocea myoblasts and pseudosciaena crocea precursor adipocytes into a cell culture plate subjected to anti-adhesion treatment for proliferation culture, spontaneously gathering to form cell spheres, and carrying out differentiation culture to obtain the cell culture meat. According to the co-culture mode provided by the invention, high-efficiency myogenic differentiation and adipogenic differentiation of myoblasts and precursor adipocytes of the large yellow croakers can be realized through proliferation culture and differentiation culture, and an in-vivo microenvironment can be effectively simulated, so that cultured meat similar to a traditional meat product in texture and flavor is produced.

Described herein are targeting moieties that can be capable of specifically targeting muscle cells and can include an n-mer motif. In some embodiments, the n-mer motif contains an RGD motif. Also described herein are vector systems, particles, polypeptides that can encode and / or contain one or more targeting moieties. Also described herein are methods of delivering a cargo to a cell, such as a muscle cell, using one or more of the targeting moieties described herein.

The invention discloses application of a JMJD6-targeted reagent in preparation of a medicine for promoting myocardial cell proliferation. The medicine can promote myocardial cell proliferation after myocardial infarction and reduce the myocardial fibrosis scar area caused by myocardial infarction. AAV9 myocardial specific overexpression virus and JMJD6 myocardial specific knockout mice are utilized, and the positive effect of JMJD6 in promotion of P1 cardiac apex resection of newborn mice and regeneration and repair of injured hearts after myocardial infarction of adult mice is disclosed for the first time; the specific mechanism is that JMJD6 depends on the activity of histone demethylase, enrichment of active modification H4R3me2a and H3R2me2s in a PDK4 promoter region is removed, transcriptional expression of the H4R3me2a and the H3R2me2s is inhibited, an impaired heart energy substrate utilization mode is stimulated to be increased and converted from fatty acid oxidation energy supply to glycolysis oxidation energy supply, and then adult myocardial cell proliferation is effectively promoted. The regeneration and repair capability of the heart after myocardial infarction is greatly improved, and a new effective target spot is provided for clinical treatment of myocardial injury.

The present disclosure describes systems and methods for cell therapy. Cells (e.g., stem cells, immune cells, cardiomyocytes, etc.) may be engineered to exhibit extended half-lives as compared to control cells (e.g., non-engineered cells). The cells may be engineered to exhibit increased proliferative activity as compared to control cells. In some embodiments, immune cells may be engineered to efficiently and specifically target diseased cells (e.g., cancer cells) while control cells are insufficient or unable to target the diseased cells. In some embodiments, stem cells or differentiated cells, such as myocardial cells, may be administered to a target tissue for enhanced tissue engineering or regenerative medicine. The engineered cells disclosed herein can be engineered ex vivo, in vitro, and in some embodiments in vivo. Engineered cells prepared ex vivo or in vitro may be administered to a subject in need thereof to treat a disease (e.g., myeloma or solid tumor). The engineered cell may be autologous to the subject. Alternatively, the engineered cell may also be allogeneic to the subject.

The application provides an active exosome stent coating, a vascular stent and a preparation method and application, and belongs to the technical field of biomedical intervention instruments. The active exosome stent coating of the application adopts stem cell-derived myocardial cell active exosomes which are strengthened by active components of traditional Chinese medicine. Compared with commercial myocardial cells, the stem cell-derived myocardial cells have more significant effects of promoting blood vessels and tissue repair and regeneration, and stronger cytokine secretion capacity. The preparation method of the active exosome stent coating of the application adjusts the introduction sequence and premixing mode of active components such as exosomes and drugs, and enhances the homogeneity and stability. The vascular stent prepared by using the active exosome stent coating of the application has reasonable sequential release kinetics design, can realize precise targeted regulation on human coronary artery smooth muscle cells (HCASMC) in vitro, does not affect the repair potential of endothelial cells, and solves the contradiction between traditional stents in terms of "anti-proliferation and promotion of healing".

This invention discloses the application of alismazone B acetate in the preparation of drugs for the prevention or treatment of hypertrophic cardiomyopathy and its related symptoms. This invention is the first to propose the use of alismazone B acetate (AB23a) for the prevention or treatment of hypertrophic cardiomyopathy. The invention utilizes AB23a to directly treat cardiomyocytes obtained from directed differentiation of human embryonic stem cells in vitro, finding that AB23a treatment significantly inhibits the hypertrophic phenotype of human embryonic stem cell-cardiomyocytes. Feeding mice with hereditary hypertrophic cardiomyopathy caused by gene mutations to a diet containing AB23a showed that AB23a significantly alleviated pathological myocardial hypertrophy and improved cardiac function in mice. AB23a can be used to prepare drugs against hereditary hypertrophic cardiomyopathy, providing a new approach and method for treating hypertrophic cardiomyopathy. AB23a is the most important medicinal component of the traditional Chinese medicine Alisma plantago-aquatica, is safe for organisms, and has good clinical application prospects.

The invention belongs to the technical field of medical information processing, and particularly discloses a regression model establishment method and system for detecting related indexes of myocardial cells of Wuzhishan pigs by using blood biochemical indexes, and the method comprises the following steps: collecting blood and heart tissue samples of the Wuzhishan pigs at different month ages, detecting the blood biochemical indexes including liver function, blood fat and blood sugar indexes, and establishing a regression model for detecting the related indexes of myocardial cells of the Wuzhishan pigs. Related indexes of myocardial cells; analyzing the index expression quantity difference, and screening significant difference indexes; then calculating the correlation between the remarkably different blood biochemical indexes and myocardial cell related indexes, and determining high-correlation blood biochemical indexes; and finally, constructing a first version of multiple regression model by respectively taking the myocardial enzyme index and the myocardial cell related index as dependent variables and the high-correlation blood biochemical index as an independent variable, removing outliers and updating the sample set on the basis of the first version of multiple regression model, and constructing a second version of multiple regression model by utilizing the new sample set, and on the basis of the second version of multiple regression model, constructing a third version of multiple regression model by adopting a stepwise regression method. According to the method, related indexes of myocardial cells can be accurately deduced through blood biochemical indexes, and support is provided for Wuzhishan pig heart disease research and model animal research and development.

The invention discloses a PH response type modified polydopamine nano preparation loaded with icariin and application of the PH response type modified polydopamine nano preparation in myocardial ischemia resistance, and belongs to the technical field of biological medicine. The nano preparation takes polydopamine (PDA) as a carrier core, the carrier core is modified by methoxy polyethylene glycol (mPEG) and then loaded with icariin (ICA), and the nano preparation is named as mPEG-PDA (at) ICANPs; the preparation process comprises the steps of synthesis of mPEG-OTs, synthesis of mPEG-EDA, synthesis of PDA, preparation of mPEG-PDANPs and preparation of mPEG-PDA (at) ICANPs, under the optimal condition, the particle size of the preparation is 179.6 + / -0.432 nm, PDI is 0.130 + / -0.004, the Zeta potential is 23.4 + / -0.436 mV, the stability is good after the preparation is stored in a dark place at 4 DEG C for 30 days, the ICA drug loading capacity is 14.6 + / -1.08%, the encapsulation efficiency is 64.37 + / -2.31%, and the drug cumulative release rate reaches 73.31 + / -1.64% (pH response drug release) in an environment with the pH value of 6.5 for 72 hours. An in-vitro H9c2 cell OGD model experiment proves that the preparation can remarkably improve the survival rate of ischemic myocardial cells, inhibit apoptosis and reduce LDH release, and the effect of the preparation is superior to that of free ICA. The invention provides an efficient targeting drug delivery system for resisting myocardial ischemia, and has important clinical application value.

The invention relates to a method for producing an animal model of heart failure. The method comprises the step of weakening or deleting DDB1 protein function in myocardial cells of the animal model. The present application demonstrates that nuclear DDB1 co-agglomerates with MEF2C to control NAD + biosynthesis as well as ion homeostasis genes in the heart, and the lack of which results in the development of HFpEF. Development of HFpEF in a'double strike 'mouse model can be reversed through AAV-mediated DDB1 overexpression in myocardial cell nucleuses. Therefore, it is detected that DDB1 coordinates NAD + biosynthesis and ion homeostasis to protect the heart from being affected by ejection fraction retention heart failure caused by obesity, and the scheme of the application has therapeutic significance on treatment of obesity / diabetes HFpEF.

The application relates to the field of myocardial ischemia-reperfusion injury drugs, and discloses application of Gualou Xiebai Baijiu decoction in preparation of myocardial ischemia-reperfusion injury drugs. The myocardial ischemia-reperfusion injury drugs inhibit the GSK-3beta / Drp1-mediated mitochondrial fission pathway by targeting Akt protein, maintain the dynamic balance of mitochondrial dynamics, and play a myocardial protection role. The drugs can promote Akt phosphorylation activation, inhibit GSK-3beta activity, down-regulate Drp1 protein Ser616 site phosphorylation, up-regulate Ser637 site phosphorylation, reduce Drp1 translocation and aggregation to the outer membrane of mitochondria, and simultaneously up-regulate the expression of mitochondrial fusion proteins Mfn1 and Mfn2. The drugs can maintain the structural integrity of mitochondria, improve the mitochondrial membrane potential and ATP content, improve myocardial cell energy metabolism, regulate the expression of apoptosis-related proteins to inhibit myocardial cell apoptosis, improve the cardiac systolic function after ischemia-reperfusion, reduce the myocardial infarction area, reduce the serum myocardial injury marker level, and regulate the oxidative stress state.

The invention belongs to the technical field of medicines, and particularly relates to application of muscone in preparation of a medicine for preventing or treating aortic dissection and the medicine. The invention relates to application of muscone in preparation of a medicine for preventing or treating aortic dissection. The medicine comprises one or more of the following effects: inhibiting aortic dilatation and dissection; aortic dilatation and dissection rupture are inhibited; the infiltration of macrophages in the aorta is inhibited; the apoptosis of aortic smooth muscle cells is inhibited; the effect of reducing inflammatory cytokines in the aorta is achieved; retrogressive lesions of the aortic medial membrane are inhibited; the degradation of the aortic dissection extracellular matrix is inhibited.

The application provides an antisense oligonucleotide Jag-i9 ASO and application thereof, relates to the technical field of biological medicine, and the antisense oligonucleotide Jag-i9 ASO has the sequence of 5'-ACTGGGCCCTGCACCTGA-3'. By providing the antisense oligonucleotide of a specific sequence, the binding site of target heterogeneous ribonucleoprotein K and the Jag2 gene is targeted, the expression of the pro-inflammatory Jag2 subtype is inhibited, the Jag2 gene splicing site can be accurately targeted, the heterogeneous ribonucleoprotein K binding function is specifically blocked, a targeted intervention means is provided for the treatment of myocardial ischemia-reperfusion injury, the generation of the pro-inflammatory subtype is inhibited by efficiently and accurately regulating the alternative splicing of a specific gene, myocardial cell apoptosis and inflammatory response are reduced, myocardial function is improved, and a new approach is provided for the prevention and treatment of myocardial ischemia-reperfusion injury, the treatment effect is improved, and the advantages of reducing side effects are achieved.

The application provides a method for constructing an animal model of dilated cardiomyopathy and application, belongs to the technical field of biological medicine and animal genetic model construction, provides a new zebrafish model of dilated cardiomyopathy, is constructed by specifically overexpressing a truncated dnajb6b gene long isoform fragment in zebrafish myocardial cells, the nucleotide sequence of the gene fragment is shown as SEQ ID NO. 1, and the method for constructing the zebrafish model of dilated cardiomyopathy and application are provided, and it is further found that 4-phenylbutyric acid is applied to the preparation of a drug for treating dilated cardiomyopathy.

The invention discloses application of isobutyrate in construction of a heart failure cell model, and relates to the technical field of biology. By innovatively applying isobutyric acid or isobutyrate, a new heart failure cell model is constructed. The model treats myocardial cells by means of isobutyrate with the concentration of 0.5-5 mM, the heart failure phenotype can be efficiently induced, the effect of the concentration of 5 mM is optimal, expression of core heart failure marker genes such as Nppa, Nppb and Myh7 can be stably up-regulated, meanwhile, the area of the myocardial cells is remarkably increased, and the heart failure pathological characteristics are met. Compared with a traditional angiotensin II and other neurohormone induction model, the invention provides a non-neurohormone-dependent brand-new heart failure cell model construction path, focuses on metabolic disorder related heart failure inducements, makes up for the defect of single mechanism of the existing model, and provides a new heart failure cell model construction path. A unique tool is provided for researching myocardial damage caused by abnormal metabolism or intestinal flora metabolites.

The invention relates to the technical field of biological medicine, in particular to guanosine oxidation piRNA-014733, antisense nucleotide and application of the guanosine oxidation piRNA-014733 and the antisense nucleotide. The guanosine oxidation piRNA is named as o8G piRNA-014733, the guanosine oxidation piRNA is related to the regulation and control of myocardial ischemia reperfusion injury and myocardial cell ferroptosis, and the nucleotide sequence of the o8G piRNA-014733 gene is shown as SEQ ID NO. 1. The antisense nucleotide sequence of the o8G piRNA-014733 is as shown in SEQ ID NO. 2, and the antisense nucleotide sequence is as shown in SEQ ID NO. The expression of the o8G piRNA-014733 provided by the invention in heart tissues suffering from ischemia reperfusion injury and myocardial cells suffering from ferroptosis is remarkably up-regulated, and the o8G piRNA-014733 antisense nucleotide provided by the invention can be used for down-regulating the expression level of the o8G piRNA-014733 and inhibiting the ferroptosis of the myocardial cells.

This invention discloses a biomimetic nanocomposite, its preparation method, and its application in the preparation of products for treating atherosclerosis, belonging to the field of pharmaceutical preparation technology. The biomimetic nanocomposite is an Ir-TiO2 metal nanozyme encapsulated in an M2 macrophage membrane. This invention prepares a structurally biomimetic nanocomposite by coating Ir-TiO2 nanoparticles with an M2 macrophage membrane. After intravenous injection, the formed biomimetic nanocomposite actively targets endothelial cells in atherosclerotic lesions, releasing Ir-TiO2 antagonistically into the cytoplasm of plaque-containing endothelial cells and inflammatory macrophages. Once Ir-TiO2 reaches the lesion site, it exerts an enzymatic effect to achieve anti-inflammatory activity and promotes cholesterol excretion from inflammatory cells such as macrophages and smooth muscle cells at the lesion site, reducing intracellular lipid deposition, reducing foam cell formation, and promoting plaque growth. This nanotherapy can effectively prevent the progression of inflammation in atherosclerotic lesions and alleviate atherosclerosis.

The invention provides a potential therapeutic target for cardiac hypertrophy and heart failure, finds that the cardiac hypertrophy caused by pressure load can be obviously relieved by using adeno-associated virus (AVV9) as a carrier myocardial cell specific overexpression Ces1d gene, and finds that the Ces1d relieves the cardiac hypertrophy by promoting fatty acid oxidation; and a potential target and a new strategy are provided for heart failure treatment. According to the invention, Ces1d is taken as a regulation target, and the expression level of Ces1d is regulated, so that the fatty acid oxidation of myocardial cells can be obviously promoted, and the expression of fatty acid oxidation related genes such as Cpt1a, Cpt1b, Cpt2, Acadm, Acadvl and Acox1 can be up-regulated, thereby optimizing the utilization mode of a myocardial energy metabolism substrate; meanwhile, mitochondrial dysfunction and mitochondrial generation damage induced by pressure load can be improved. Therefore, the regulation strategy taking the Ces1d as the action target and the AVV9 as the carrier provides a new gene therapy technical approach for prevention and treatment of cardiac hypertrophy and related cardiovascular diseases, and has a good application prospect and a remarkable clinical potential value.

The application provides application of Trapidil in preparation of a drug for preventing and / or treating doxorubicin-induced organ toxicity, and belongs to the technical field of biological medicines.The application discloses that Trapidil plays an organ protection role by activating a cAMP / PKA / CREB signal axis and driving two parallel downstream effect channels: on the one hand, up-regulating an NRF2-GPX3 positive feedback loop to inhibit doxorubicin-induced myocardial cell pyroptosis and glomerular podocyte pyroptosis; and on the other hand, activating an NRF2 / HO-1 channel to inhibit myocardial cell apoptosis and glomerular podocyte apoptosis.In-vivo and in-vitro experiments prove that Trapidil can improve doxorubicin-induced cardiac dysfunction and kidney function damage, reduce histopathological damage, reduce the level of oxidative stress, inhibit the pyroptosis and apoptosis of myocardial cells and glomerular podocytes, and does not affect the antitumor effect of doxorubicin.The application provides a new drug strategy for doxorubicin chemotherapy-induced multi-organ toxicity.

The invention provides a hydrogel-biological sponge composite material as well as a preparation method and application thereof, and belongs to the technical field of biological materials. The drug-loaded hydrogel is adopted to load the anti-inflammatory drug, inflammation caused by skeletal muscle injury is relieved, and the skeletal muscle healing process is promoted; a defect area is rapidly filled, and muscle-derived stem cell differentiation and muscle fiber formation are promoted; a topological structure of a skeletal muscle extracellular matrix is highly simulated by adopting biological sponge, muscle cells are effectively guided to be directionally arranged along fibers, and further myotube fusion and differentiation are promoted; the specific surface area is larger, sufficient living space is provided for cells, and adhesion and proliferation of the cells are facilitated; the biological sponge is good in mechanical property, so that the prepared hydrogel-biological sponge composite material is good in supporting property, and skeletal muscle repair is facilitated.

The application discloses a kind of mitochondrial quality control detection methods, the present application relates to mitochondrial quality control detection technical field, operating steps include preparation sample cell suspension, fluorescent dye labeling, cardiomyocyte separation, establish myocardial cell damaged model and detect mitochondrial membrane potential situation.This mitochondrial quality control detection method can simultaneously carry out multi-parameter, rapid quantitative analysis and sorting, measure fast, measure the multi-parameter characteristics of each cell, while carrying out cell characteristic analysis, can separate out the cell of specified characteristics, so as to further culture, cloning, observation or carry out mitochondrial fragmentation test to specific cell, establish myocardial cell damaged model using doxorubicin, the mitochondrial membrane potential situation of normal myocardial cell and damaged myocardial cell obtained by using JC-1 mitochondrial membrane potential fluorescent probe detection is verified the detection quality of this mitochondrial quality control detection method.

Described herein are targeting moieties that can be capable of specifically targeting muscle cells and can include an n-mer motif. In some embodiments, the n-mer motif contains an RGD motif. Also described herein are vector systems, particles, polypeptides that can encode and / or contain one or more targeting moieties. Also described herein are methods of delivering a cargo to a cell, such as a muscle cell, using one or more of the targeting moieties described herein.

This invention discloses the application of lipoic acid analog formulations in the preparation of anti-cardiomyocyte senescence products. The lipoic acid analog DMAE-LA is N-(2-(dimethylamino)ethyl)-5-(1,2-dithiopentane-3-yl)pentanamide, with a concentration of 2-25 μM. DMAE-LA pretreatment effectively reduces intracellular ROS, improves mitochondrial function, inhibits the overexpression of p21 and HMGB1, and restores Lamin B1 levels, thereby alleviating the senescent manifestations of cardiomyocytes. DMAE-LA reduces H₂S oxidative depletion by inhibiting ROS generation and may promote H₂S synthase activity, increasing endogenous H₂S levels and further enhancing cellular antioxidant capacity. In summary, DMAE-LA can significantly inhibit cardiomyocyte senescence through multiple antioxidant mechanisms and organelle function protection, providing a potential intervention strategy for targeting cellular senescence in cardiovascular diseases.

The invention relates to an adenovirus associated virus 9 (AAV9)-based viral particle, for use in a method of treatment of a heart disease, whereby said viral particle is administered to the heart. The invention further relates to a pharmaceutical composition comprising the AAV9-based viral particle, and to methods of producing the AAV9-based viral particle.

The invention discloses a motion intervention heart failure repair method based on Lgmn signal regulation and control, and relates to the technical field of heart failure treatment. According to the method, through aerobic exercise training (AET) with specific parameters, expression of Legumain (Lgmn) genes in macrophages is regulated in a targeted mode, the interburial effect of the macrophages is enhanced, then cell communication between the macrophages and cardiac muscle cells is enhanced, removal of the vertical death cardiac muscle cells is promoted, myocardial fibrosis and inflammatory response are relieved, and the effect of treating myocardial fibrosis is achieved. Finally, ventricular remodeling and heart functions of chronic heart failure (CHF) mice are improved. Experimental verification shows that the exercise intervention method can significantly improve the left ventricular ejection fraction (LVEF) and shortening fraction (FS) of CHF model animals, reduce the left ventricular end-of-systole inner diameter (LVESD), reduce myocardial cell apoptosis and necrosis, and promote inflammation regression. Drug intervention is not needed, safety is high, operation is easy and convenient, and a new effective way is provided for clinical rehabilitation treatment of heart failure.

Provided herein are novel reprogrammed smooth muscle cells (rSMCs) and methods of making and using the cells for the treatment of ischemia. The rSMCs are produced by culturing a fibroblast with an all-trans-retinoic acid (ATRA) under conditions that produce the rSMC from the fibroblast, wherein the fibroblasts are genetically modified to overexpress myocardin. The rSMCs offer advantages over currently available regenerative vascular therapies by promoting vascular perfusion in a recipient subject. In particular, the rSMCs can increase neovascularization of both small and large vessels.

The invention belongs to the technical field of biological medicines, and particularly relates to application of przewatanshinone A in preparation of a medicine for treating anti-tumor medicine cardiotoxicity. The traditional Chinese medicine-induced cardiotoxicity disclosed by the invention is cardiotoxicity caused by anthracycline drugs. Experiments prove that przewatanshinone A has a multi-target synergistic effect and can remarkably inhibit myocardial cell oxidative stress, relieve inflammatory response and protect myocardial cell functions, so that cardiotoxicity caused by anthracycline drugs is effectively prevented and treated, and a brand-new solution is provided for clinical prevention and treatment of cardiotoxicity caused by anthracycline drugs.

The invention relates to application of a Nexilin overexpression recombinant vector in preparation of a medicine for treating MIRI, and belongs to the technical field of biological medicine. In order to solve the problems of insufficient intervention of a core pathological mechanism and limited treatment effect of the existing MIRI treatment means, the invention provides application of a Nexilin overexpression recombinant vector in preparation of MIRI treatment medicines. The invention proves that the Nexilin overexpression vector can effectively improve myocardial ischemia-reperfusion injury for the first time, can remarkably improve the cardiac function of a mouse suffering from myocardial ischemia-reperfusion injury, reduce the content of myocardial injury markers, reduce the myocardial infarction area, restore the expression balance of Bcl-2 family proteins and inhibit myocardial cell apoptosis by up-regulating Bcl2 expression and down-regulating Bax expression, and has the advantages of being capable of improving myocardial ischemia-reperfusion injury, and being used for treating myocardial infarction. The protection effect on ischemia reperfusion myocardium is realized from multiple levels, and a brand new technical means and experimental basis are provided for clinically developing targeted therapeutic drugs for myocardial ischemia reperfusion injury.

The present application provides a method for regulating calcium ion influx of myocardial cells by modifying any one or more of the amino acid residues in the combination of ESSE at positions 2061-2064 in the amino acid sequence corresponding to SEQ ID No. 1 of the mammalian L-type calcium channel protein, and a calcium channel regulator. The present application also provides a pharmaceutical composition for treating cardiovascular diseases, which comprises a regulator of any one or more of the amino acid residues in the combination of ESSE at positions 2061-2064 in the amino acid sequence corresponding to SEQ ID No. 1 of the mammalian L-type calcium channel protein. The present application also provides a method for screening potential substances for treating cardiovascular diseases.

The objective is to provide a method for improving facial aging, utilizing a novel mechanism different from known methods for improving facial aging, such as loss of firmness and sagging, and from existing agents for improving facial aging. [Solution] Focusing on the relationship between skin sagging and the arrector pili muscles, this invention provides a cosmetic method to improve sagging, wrinkles, or hollowness by activating or proliferating arrector pili muscle cells.

The application discloses application of a GPR146 inhibitor in preparation of a drug for treating wet age-related macular degeneration. The application finds that GPR146 is significantly up-regulated in expression in a mouse model of laser-induced CNV and a mouse model of subretinal fibrosis. In mice, shRNA is used to knock down GPR146, thereby significantly inhibiting CNV, subretinal fibrosis and inflammation. In an in-vitro experiment, siRNA targeting GPR146 can inhibit the in-vitro neovascular function of endothelial cells, such as proliferation, migration and tube formation, and reduce immune cell adhesion and transendothelial cell migration. In addition, targeting GPR146 can also inhibit the expression of TGF-beta, Fibronectin (FN), alpha-SMA, Col1A, MMP9 and other fibrosis-promoting molecules by endothelial cells. Meanwhile, targeting GPR146 can also inhibit the proliferation and migration of smooth muscle cells and reduce the expression of the above fibrosis-promoting molecules. The above results all show that targeting GPR146 can significantly inhibit CNV formation, inflammation and subretinal fibrosis, and has good therapeutic effect.