55 results about "Myocardial hypertrophy" patented technology

The application discloses application of a BLM helicase inhibitor in treating myocardial hypertrophy. The application firstly finds that the BLM helicase inhibitor ML216 can significantly inhibit cardiac hypertrophy and myocardial cell fibrosis, thereby providing a new drug for treating myocardial cell hypertrophy diseases in the field, and providing practical experimental evidence and scientific basis for treating myocardial cell hypertrophy diseases, and having a good application prospect in treating myocardial hypertrophy and / or cardiac hypertrophy.

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 biological medicine, and particularly provides application of flufenidone in preparation of a medicine for preventing or treating left heart failure. The research finds that the flufenidone has the effects of relieving myocardial cell hypertrophy under a heart failure cell model and relieving myocardial hypertrophy, fibrosis and heart function deterioration of an aortic constriction animal model. According to the present invention, further research results show that fluorofenidone is directly combined with SERCA2a through Q758, D812 and E917 residues of SERCA2a so as to inhibit recognition, combination and polyubiquitination effects of WWP1 on SERCA2a, such that the protein level and the activity of SERCA2a are stabilized so as to achieve the chronic left heart failure treatment purpose. Therefore, the flufenidone serving as an active ingredient has good application prospect and application value in research and development of novel medicines for treating chronic left heart failure.

The invention relates to the technical field of traditional Chinese medicine preparations, in particular to an anti-heart-failure traditional Chinese medicine composition and a pharmaceutical preparation. The traditional Chinese medicine composition comprises sun-dried ginseng, radix ophiopogonis, schisandra chinensis, American ginseng, pseudo-ginseng and poria cocos. The traditional Chinese medicine composition for resisting heart failure and the medicinal preparation provided by the invention can relieve myocardial damage and load of patients with heart failure and relieve myocardial hypertrophy and fibrosis, so that the heart function of the patients with heart failure is effectively improved.

The application discloses application of a lipoic acid analogue in preparation of a product for relieving myocardial cell hypertrophy, and the lipoic acid analogue DMAE-LA is N -(2-(dimethylamino)ethyl)-5-(1,2-dithiopentyl-3-yl)valeric amide. DMAE-LA can effectively reduce ISO-induced myocardial hypertrophy of mice, reduce heart weight index and ANP and BNP expression, and significantly improve heart function. A small dose (2-10 μM) of a lysosome-targeting lipoic acid analogue DMAE-LA can effectively improve Ang II-induced myocardial hypertrophy and oxidative stress in H9c2 cells, and the protective effect is better than that of a high dose (200-400 μM) of LA. As a new substitute of traditional LA, DMAE-LA shows great potential for prevention and treatment of cardiovascular diseases.

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.

This invention relates to the field of congenital heart disease treatment technology, and discloses the application of sapropterin in the prevention and treatment of bisphenol fluorene-induced congenital heart disease in fetuses. The congenital heart disease includes cardiac structural defects, heart failure, or cardiomyocyte lesions, specifically selected from ventricular septal defects, atrial septal defects, tetralogy of Fallot, myocardial hypertrophy, decreased cardiac ejection fraction, decreased short-axis contraction rate, cardiomyocyte ferroptosis, myocardial tissue inflammatory infiltration, or myocardial collagen fibrosis. Sapropterin is used as a direct supplement to biological tetrahydropterin (BH4). Through exogenous intervention, it precisely reverses the endogenous BH4 deficiency caused by bisphenol fluorene exposure, restores the expression of GTP cyclase 1 (GCH1) and the dynamic balance of RNA m6A, and upregulates the level of YTH domain family protein 2 (YTHDF2), thereby blocking ferroptosis signal transduction, reducing oxidative stress and inflammatory response, and inhibiting the process of myocardial tissue fibrosis at the molecular level.

This invention belongs to the field of biomedical technology, specifically involving Trmt61a The application of genes in the preparation of drugs for treating pathological myocardial hypertrophy. This invention provides... Trmt61a The application of genes in the preparation of drugs for treating pathological myocardial hypertrophy, the aforementioned Trmt61a The nucleotide sequence of the gene is shown in SEQ ID NO.1. Animal experiments have shown that knocking down... Trmt61a Gene knockdown can significantly improve cardiac contractile function after aortic arch coarctation surgery, alleviate cardiomyocyte hypertrophy, reduce the degree of cardiac fibrosis, and effectively treat pathological myocardial hypertrophy. This invention is the first to demonstrate knockdown... Trmt61a Genes can effectively improve pathological myocardial hypertrophy, providing a new drug development path and target for the prevention and treatment of this disease, and have important medicinal value and clinical application prospects.

The application discloses a kind of short peptides simulating RhoE C end, derivative and its pharmaceutical use in treating ventricular remodeling, belong to biological medicine technical field.The short peptide and derivative contain RhoE C end 200-240 linear function domain, can be combined and activated WWP2, remove HGS self-inhibition, start endosome-lysosome degradation pathway.Short peptide sequence is as SEQ ID NO.1, derivative can be coupled with TAT, T7 or RVG membrane penetrating peptide (SEQ ID NO.2-4), and endocytosed to myocardial cell by caveolin high efficiency delivery.The application solves the defects that existing anti-ventricular remodeling drug inhibits protective autophagy flow, and the ability of eliminating toxic protein is limited, can efficiently eliminate damaged mitochondria and misfolded protein, inhibits myocardial hypertrophy, fibrosis, improves cardiac remodeling, provides safe and effective treatment strategy for related diseases.

This invention belongs to the field of biomedical engineering and relates to the application of SnoRNA Gm26330 as a biomarker and therapeutic target for myocardial hypertrophy. This invention provides a biomarker for myocardial hypertrophy, snoRNA Gm26330, the nucleotide sequence of which is shown in SEQ ID No. 1. In vitro and in vivo experiments have shown that SnoRNA Gm26330 can inhibit myocardial hypertrophy and has a protective effect against myocardial damage caused by myocardial hypertrophy. SnoRNA Gm26330 has potential value in the preparation of drugs for the prevention and treatment of related heart diseases.

The invention provides an application of up-regulated human enoyl coenzyme A delta isomerase 2 (ECI2) in preparation of a medicine for protecting a cardiac function. It is found for the first time that up-regulation of ECI2 promotes degradation of crotonyl coenzyme A by consuming a crotonyl donor (crotonyl coenzyme A) and effectively inhibits crotonyl modification, so that the heart function and myocardial hypertrophy can be effectively improved, and then the heart function protection effect on pressure overload heart diseases and heart failure is achieved. The above findings indicate a huge potential of upregulating ECI2 in the prevention and / or treatment of pressure overload heart diseases and heart failure.

The application discloses a plant extraction compound for reducing blood pressure, a preparation method and application thereof. The compound is composed of high-purity silybin extract and a specific fusion polypeptide through molecular self-assembly. The sequence of the fusion polypeptide is shown in sequence SEQ ID NO:1, which innovatively integrates cell membrane penetration function, angiotensin II receptor 1 antagonism function and hydrophobic drug binding function. The core of the application is that through polypeptide-mediated active targeting, silybin is accurately delivered to the diseased blood vessel area, and the double synergistic mechanism of upstream ACE inhibition and downstream receptor blocking of the renin-angiotensin-aldosterone system is realized. In-vivo pharmacodynamic experiments prove that compared with single components, the compound can produce more significant and persistent antihypertensive effect, and can effectively reverse myocardial hypertrophy and fibrosis caused by hypertension, and show excellent synergistic therapeutic effect and target organ protection ability.

This invention belongs to the field of pharmaceutical technology, and relates to diphenylmethane derivatives, their preparation methods, and applications. The diphenylmethane derivative is a compound represented by Formula I, its optical isomer, or a pharmaceutically acceptable salt thereof: wherein X is CH2; Y is selected from: -NH-, -CO-, -NHCONH-. The diphenylmethane derivative of this invention is stable, easy to store, and readily prepared, exhibiting good feasibility. It demonstrates outstanding in vitro and in vivo efficacy and good safety profile when used to prepare anticardioprotective drugs (for heart failure and myocardial hypertrophy).

The invention relates to a viral vector carrying a Prrg3 gene expression cassette and application thereof in treating diseases. Specifically, the invention relates to a Prrg3 gene expression cassette, a virus vector carrying the Prrg3 gene expression cassette and application of the virus vector in treatment of heart failure, cardiac hypertrophy, hypertension, overweight, obesity, diabetes, fatty liver, hyperlipidemia and other diseases, and the virus vector is especially suitable for ejection fraction retention heart failure patients with one or more diseases. The application provides a new thought and strategy for clinical treatment of ejection fraction retention heart failure and complications thereof, and has a wide application prospect.

The application relates to application of siRNA-OTUB1 in preparation of drugs for preventing or treating myocardial cell hypertrophy, and belongs to the biomedical technical field.The nucleotide sequence of the OTUB1 gene is shown as SEQ ID NO.1, and the targeted nucleotide sequence of the siRNA-OTUB1 for specifically interfering with the expression of the OTUB1 gene is shown as SEQ ID NO.2 or SEQ ID NO.3.The application innovatively proposes a strategy for preventing or treating myocardial cell hypertrophy by taking deubiquitinase OTUB1 as a core target point and by interfering with the expression thereof.In a myocardial cell experiment of a milk rat, the application of the designed siRNA-OTUB1 can effectively reduce the expression levels of OTUB1 mRNA and OTUB1 protein, and further reduce the degree of myocardial cell hypertrophy.Based on the finding, the OTUB1 gene can be developed as a novel treatment target point for myocardial cell hypertrophy, is used for designing a targeted drug, and provides a new technical thought for precise treatment of myocardial hypertrophy.

The invention relates to medical application of IRF9 in prevention and treatment of trastuzumab (TRZ) cardiotoxicity, and belongs to the technical field of biological medicine. The invention reveals that the expression of the interferon regulatory factor 9 (IRF9) in the TRZ cardiotoxic myocardial tissue is up-regulated for the first time, and myocardial damage is aggravated by promoting pyroptosis of myocardial cells. On the basis, the invention provides the IRF9 as a diagnostic marker of TRZ cardiotoxicity, and provides an application of an IRF9 low expression vector or small interfering RNA (siRNA) in preparation of drugs for preventing or treating TRZ cardiotoxicity. Animal experiments show that cardiac function decline, cardiac hypertrophy and fibrosis caused by TRZ can be remarkably improved by myocardial cell specific low-expression IRF9. The invention provides a new target spot and an intervention strategy for clinical prevention and treatment of TRZ cardiotoxicity.

The invention belongs to the technical field of biological medicines, and particularly relates to a compound Atovaquone for treating cardiomyopathy, and the cardiomyopathy refers to all diseases causing myocardial structure and dysfunction, including secondary cardiac hypertrophy / heart failure and primary hypertrophic cardiomyopathy. The compound can be prepared into granules, capsules, powder, tablets and injection preparations together with another active ingredient which is different from the compound shown in the formula I and has the functions of enhancing the heart function, expanding peripheral blood vessels, reducing myocardial oxygen consumption and the like, and pharmaceutically acceptable auxiliary materials are added.

The invention relates to a quinic acid salicin ester derivative extracted from shiny feet, a method and application. The quinic acid salicin ester derivative is at least one of a compound 1 and a compound 2. The compound 1 and the compound 2 can be used for preparing medicines or products for preventing or treating myocardial hypertrophy diseases; and when the concentration of the compound 1 and the compound 2 is less than 50 [mu] mol / L, the compound 1 and the compound 2 have no obvious toxicity to cells and show higher biological safety. The invention provides a new choice for development of a cardiac hypertrophy inhibitor.

The invention provides application of dracocephalum moldavica total flavonoids in preparation of a medicine for preventing and / or treating heart failure with preserved ejection fraction, and belongs to the technical field of biological medicine. After a heart failure model mouse with reserved ejection fraction is constructed and dracocephalum moldavica general flavone is administrated, research finds that compared with an HFpEF model group mouse, the myocardial cell damage degree of the dracocephalum moldavica general flavone group mouse is obviously reduced, the myocardial hypertrophy is obviously reduced, and the myocardial hypertrophy is obviously reduced. The total flavonoids of dracocephalum moldavica can significantly reduce pathological cardiac hypertrophy and myocardial fibrosis of HFpEF model mice, improve cardiac diastolic function, and reduce the degree of liver cell injury and lipid metabolism imbalance, thereby preventing and / or treating heart failure with ejection fraction retention.

The invention discloses application of a membrane-bound O-acyltransferase structural domain 7 (Mboat7) in preparation of a medicine for treating myocardial hypertrophy, and belongs to the technical field of biology. Research results show that in a mouse cardiac hypertrophy model, compared with a control group mouse, heart weight / body weight, lung weight / body weight, cardiac muscle cell cross sectional area and fibrosis of a cardiac muscle cell specific Mboat7 gene overexpressed mouse are all remarkably reduced, and the cardiac systolic function is remarkably improved; the overexpressed Mboat7 gene can relieve isolated cell myocardial hypertrophy induced by angiotensin II. Particularly, overexpression of the Mboat7 gene can improve damage of mitochondria in myocardial tissue of a cardiac hypertrophy mouse. The results show that the Mboat7 gene overexpression relieves the disease progress of the pathological cardiac hypertrophy, and the Mboat7 or the expression promoter thereof can be used for preparing the medicine for preventing, relieving and / or treating the pathological cardiac hypertrophy.

The invention discloses a function and application of a lysine deficiency type protein kinase 2 inhibitor in inhibition of ventricular remodeling, and belongs to the field of functions and application of genes. According to the invention, the mutual relation between the expression of the WNK2 and the ventricular remodeling is determined, and the research result shows that the expression of the WNK2 is obviously improved compared with that of a normal group in a model with pathological ventricular remodeling; the ventricular remodeling including cardiac hypertrophy, fibrosis and heart function decline is remarkably relieved by inhibiting the expression of the WNK2, and the ventricular remodeling process is remarkably intensified and the heart function is deteriorated by promoting the overexpression of the WNK2. The WNK2 can be used as a drug target and used for screening drugs for protecting heart functions, resisting myocardial fibrosis and / or preventing, relieving and / or treating ventricular remodeling and related heart diseases, and an inhibitor of the WNK2 can be used for developing drugs for protecting heart functions, inhibiting ventricular remodeling and preventing, relieving and / or treating ventricular remodeling related diseases. And an effective new way is provided for clinical treatment of ventricular remodeling.

The invention relates to the technical field of biological medicine, and particularly discloses a membranous organelle nano-vesicle for preventing and treating myocardial hypertrophy and a preparation method and application thereof, and the membranous organelle nano-vesicle comprises endoplasmic reticulum extracted from mammal liver tissue and nano-scale vesicles which are obtained after ultrasonication treatment and have a calcium ion buffering function. The liver-derived endoplasmic reticulum nano-vesicles and the derivatives thereof are extracted and are directly physically fused with the myocardial cell endoplasmic reticulum, so that the technical spanning from chemical signal regulation to organelle function reconstruction is fundamentally realized, the calcium pump activity of SERCA2a is accurately and efficiently enhanced, the endoplasmic reticulum calcium homeostasis is directly repaired, and the liver-derived endoplasmic reticulum nano-vesicles and the derivatives thereof are used for preparing the myocardial cell endoplasmic reticulum nano-vesicles. Meanwhile, energy metabolism is synergistically improved, and cell apoptosis is inhibited, so that the pathological process of myocardial hypertrophy is remarkably reversed in an animal model, and the compound has excellent biological safety and industrialization potential due to the biogenic characteristic of the compound.

The invention discloses an application of a composition of a CD36 inhibitor and a PDK4 inhibitor in preparation of a medicine for treating HFpEF, and the CD36 inhibitor and the PDK4 inhibitor are combined for use and are used for cooperatively regulating and controlling myocardial metabolism reprogramming so as to treat the HFpEF. Through combined application of the CD36 inhibitor and the PDK4 inhibitor, the effects of the combined scheme on a plurality of key indexes such as improvement of the heart diastolic function of an HFpEF mouse, improvement of exercise tolerance, reversal of cardiac hypertrophy, reduction of pulmonary congestion and myocardial fibrosis and the like are remarkably superior to those of any single-drug treatment group of SSO or DCA, and synergistic treatment is achieved.

The invention relates to a myocardial hypertrophy cause classification method and device based on multi-modal data fusion, and the method comprises the following steps: obtaining multi-modal data of a to-be-classified object, the multi-modal data comprising a heart MRI image, an echocardiogram, an electrocardiogram and clinical text information; performing standardization preprocessing on the modal data, and extracting pathogenesis specificity features corresponding to the modal data; performing adaptive weighting and aggregation on the etiological specificity features corresponding to the modal data through a middle-term fusion strategy based on an attention mechanism to obtain fusion features; and performing end-to-end classification on the fusion features by using a deep learning model to obtain a myocardial hypertrophy cause classification result. Compared with the prior art, the method provided by the invention solves the problems of insufficient single-mode discrimination and difficult fusion of cross-mode isomerism, and has the advantages of high recognition accuracy, high efficiency, strong robustness and the like.

This invention belongs to the field of biomedical technology, specifically involving knockout. Slc16a4 Gene or repression Slc16a4 The application of gene expression reagents in the preparation of drugs for the prevention and / or treatment of HFpEF. This invention involves administering AAV9 virus-packaged Slc16a4 shRNA to mice. Results showed that injection of Slc16a4 shRNA significantly improved diastolic dysfunction, reduced blood pressure, improved exercise tolerance, and alleviated myocardial hypertrophy and cardiac fibrosis in HFpEF mice, thus achieving treatment for HFpEF. This invention provides a highly efficient targeted... Slc16a4 Gene intervention tools provide key technical support for HFpEF-related gene function research and the development of targeted intervention products, and have significant scientific value and application prospects.

The invention belongs to the technical field of biology, and particularly relates to related tRF for detecting hypertrophic cardiomyopathy and a detection method and application thereof. The invention provides a marker for hypertrophic cardiomyopathy, the marker is CHAtRF, and the nucleotide sequence of the marker is as shown in SEQ ID NO: 1. The CHAtRF antisense nucleotide CHAtRF antiagomir can be used as an active ingredient in a product for treating hypertrophic cardiomyopathy. By using the CHAtRF antiagomir, the expression of CHAtRF in the heart can be inhibited, pathological myocardial hypertrophy can be remarkably inhibited, the fibrosis area can be reduced, and the effect of improving the heart function can be achieved, so that the purpose of preparing the medicine for preventing and / or treating hypertrophic cardiomyopathy by using the CHAtRF antiagomir as a novel gene therapy technology is achieved; and a new drug action target is provided for treatment of heart diseases related to hypertrophic cardiomyopathy.

This invention discloses the application of apolipoprotein M in the preparation of a medicament for treating heart failure with preserved ejection fraction (HFpEF). The medicament comprises apolipoprotein M and a medically acceptable carrier or excipient. Animal experiments have shown that liver-specific overexpression of ApoM improves diastolic dysfunction, myocardial hypertrophy, and myocardial fibrosis in HFpEF mice, while liver-specific knockdown of ApoM exacerbates this pathological process. This provides a novel treatment strategy for HFpEF and also offers a theoretical basis for ApoM as a biomarker for HFpEF.