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101
results.
Updated on
20/08/2026 [07:51:00]
Results 50 to 75 of 101
Absstract of: US20260151373A1
0000 The current methods and compositions relate to treatment of atrial fibrillation with bucindolol in patients, including patients with heart failure, after being determined to be homozygous Arg389 in the β<1 >adrenergic receptor gene.
Absstract of: CN122124244A
The invention relates to the technical field of biological medicines, in particular to application of PTPRM in treatment and/or prevention of sepsis cardiomyopathy. The application discovers that the expression level of PTPRM in heart tissue of a CLP model is remarkably reduced, and further verifies that the survival rate of the CLP model is remarkably improved after PTPRM overexpression, PAT reduction and RVFW, RVSFW, LVSFW, LVDFW, IVS-s and IVS-d increase caused by CLP modeling are also improved, in addition, the expression level of cardiac troponin (cTNT) and right ventricular wall thickness can also be reduced by overexpression of PTPRM, and the survival rate of the CLP model is remarkably improved. PTPRM can be used as a target spot for treating sepsis cardiomyopathy.
Absstract of: CN122128425A
The invention relates to the technical field of gene polymorphism detection, and discloses a venous thrombosis risk gene detection kit based on an LAMP (loop-mediated isothermal amplification) technology, which comprises primer probes used for detecting venous thrombosis risk gene polymorphism sites, detection reaction system components, a reagent A, a reagent B, a positive quality control A, a positive quality control B and a negative control, the reagent A and the reagent B respectively comprise matched primer probes and detection reaction system components, the reagent A is a 4G reaction tube, a C reaction tube, an AAG reaction tube, a G reaction tube or a T reaction tube, and the reagent B is a corresponding 5G reaction tube, a T reaction tube, a del reaction tube, an A reaction tube or a C reaction tube. According to the invention, reactions of different nucleic acid sequences are physically isolated in the independent reagent A and reagent B so as to avoid mutual interference of primer probes, meanwhile, polymerase and cresol red are utilized to convert system component change into color change, and visual output and accurate typing of multi-target amplification signals are synchronously realized under the condition of avoiding instrument assistance.
Absstract of: CN122128427A
The invention discloses a plasma protein as a biomarker for diagnosing STEMI combined hypertension and application thereof, and is characterized in that the plasma protein biomarker is CA1 and can be applied to preparation of a product for diagnosing STEMI combined hypertension; the kit has the advantages that the STEMI combined hypertension is diagnosed in an early stage by measuring the plasma protein biomarkers, an effective tool is provided for diagnosis of the STEMI combined hypertension, the detection efficiency is high, and the pertinence is strong.
Absstract of: CN122128418A
The invention belongs to the technical field of biomedicine, and discloses application of a KLF13 gene regulatory factor in great vessel arteriovenous senescence. Systematic analysis on a Klf13 gene knockout mouse shows that Klf13 is an important protection factor for maintaining the vascular homeostasis. In-vitro experiments show that the DNA damage of KLF13 knock-down cells is increased, the multiplication capacity is reduced, and the KLF13 plays a role in protecting blood vessel aging; in vascular cell types, the change of KLF13 knock-down in endothelial cells is most significant. Arteriovenous endothelium migration and tubulation function decline. The core function of KLF13 in maintaining the steady state of the blood vessel is disclosed. According to the discovery, the status of KLF13 serving as a key vascular protection factor is determined from the functional level, and dysfunction of KLF13 may be closely related to occurrence and development of vascular aging and related diseases. And theoretical and practical basis is provided for developing products for identifying senescence of vascular cells.
Absstract of: CN122104891A
The invention provides a single or combined gene marker of GFPT2, LUM, TNXB and THBS4 and application of the gene marker in risk early warning and prognosis evaluation of cardiovascular diseases, and belongs to the technical field of biomedicine. The invention provides a universal molecular marker composition which is closely associated with a common core pathological mechanism (namely myocardial fibrosis) finally causing heart failure, and the universal molecular marker composition can cross the initial causes of different cardiovascular diseases and can be used for detecting the heart failure in the early stage of irreversible fibrosis damage of myocardium. Accurate early warning and prognosis evaluation of the heart failure risk are realized, and a time window and a targeting basis are provided for early intervention. The invention finds that the four genes GFPT2, LUM, TNXB and THBS4 can be independently used or a combination of the four genes can be used as a universal biomarker for crossing different causes and specifically pre-warning a common end pathway (myocardial fibrosis) of heart failure. The invention establishes a heart failure risk prediction mathematical model which is based on the expression levels of the four genes and is suitable for wide cardiovascular patient groups.
Absstract of: US20260148848A1
0000 The disclosure relates to a combination of biomarkers comprising at least: (i-a) one biomarker selected in each of the following group of biomarkers: Patient's age, Plasma steroids, and Urinary steroids, and at least one biomarker selected in at least one of the group of biomarkers: O-methylated catecholamines, Small metabolites, and miRNA; or (i-b) one biomarker selected in each of the following group of biomarkers: Plasma steroids, Urinary steroids, and Small metabolites, and at least one biomarker selected in at least one of the group of biomarkers: Patient's age, O-methylated catecholamines, and miRNA. The combinations of biomarkers may be used for stratifying a hypertensive patient among different hypertensive diseases comprising Endocrine Hypertension (EHT), Primary Aldosteronism (PA), Pheochromocytoma/Functional Paraganglioma (PPGL), Cushing's Syndrome (CS), and Primary Hypertension (PHT).
Absstract of: EP4748932A1
The present invention refers to Annexin A8 (AnxA8) inhibitors, or pharmaceutical composition comprising thereof, for use in a method for the treatment and/or prevention of atherosclerosis. Preferably, the method comprises preventing atherosclerotic plaque formation.
Absstract of: CN122075518A
The invention belongs to the technical field of transplanted vascular remodeling diagnosis and treatment, and discloses application of a reagent for inhibiting or detecting Fasn and a medicine for preventing and/or treating transplanted vascular remodeling. Experimental research discovers that a group of novel macrophages capable of self-synthesizing lipid exist in the transplantation blood vessel reconstruction process, and Fasn is remarkably activated, so that intracellular lipid accumulation is caused, and the macrophages are promoted to be converted into foam cells. In-vitro studies show that by inhibiting the activity of the Fasn enzyme or down-regulating the expression of the Fasn enzyme, the transformation of macrophages to foam cells can be obviously inhibited, and the synthesis of lipid in cells can be reduced. Based on the discovery, the nucleic acid medicine constructed by adopting the siRNA is used for treating and/or relieving transplanted vascular remodeling. In-vivo experiments further prove that the nucleic acid medicine can remarkably inhibit intimal hyperplasia of transplanted blood vessels and reduce the neointimal/medial membrane ratio, so that the therapeutic effect is achieved. The method has a good application prospect.
Absstract of: CN122081474A
The invention belongs to the technical field of biological medicines, and discloses a new mutation c.311Ggt of a TNNT2 gene related to dilated cardiomyopathy. A. Family genetic analysis and in-vitro function verification prove that the mutation causes enhanced sensitivity of myocardial cells to doxorubicin and fragmentation of a mitochondrial network, and the mutation has pathogenicity. On the basis, the invention provides a specific detection primer pair and a kit, which are used for rapid gene diagnosis and risk assessment of dilated cardiomyopathy.
Absstract of: CN122081482A
The invention provides a poor collateral circulation biomarker UBE2L3 and application thereof, and belongs to the technical field of biomedicine. According to the application disclosed by the invention, the key effect of the UBE2L3 in inhibiting the formation of the chronic coronary artery complete occlusion collateral circulation is defined for the first time, and the 'UBE2L3-Parkin-Drpl' axis is determined as a key endogenous inhibition pathway for regulating and controlling the CTO collateral circulation. The invention provides a clear intervention target with a clear mechanism for developing a brand new precise therapy for promoting therapeutic angiogenesis, solves the problems of unstable curative effect and off-target risk caused by a wide target in a current angiogenesis promoting strategy, provides a brand new non-surgical biological treatment strategy aiming at enhancing endogenous angiogenesis ability, and has a wide application prospect. Myocardial ischemia is expected to be improved essentially, so that the risk of adverse events such as long-term myocardial infarction and heart failure is reduced.
Absstract of: CN122071740A
The invention belongs to the technical field of biological medicine and molecular biology, and particularly relates to application of carbonic anhydrase IV in prevention and treatment of coronary microangiopathy. The research proves that the carbonic anhydrase IV has the effects of maintaining the activity of human microvascular endothelial cells, promoting the development of heart microvessels and protecting the barrier function of the microvessels. It is shown that the carbonic anhydrase IV can play a role in inhibiting CMVD lesion by preventing heart microvascular density reduction and inhibiting heart microvascular permeability increase in the CMVD process, and therefore the carbonic anhydrase IV has good potential practical application value.
Absstract of: US20260139229A1
0000 Provided herein are multilineage cardiovascular organoids and methods of generating the same. In some aspects, provided herein is a system comprising a plurality of multilineage cardiovascular organoids derived from embryoid bodies. The embryoid bodies can be aggregated from pluripotent stem cells of varying genotypes. The multilineage cardiovascular organoids and systems described herein may be used for screening of agents, such as anti-cancer agents, for cardiotoxicity.
Absstract of: CN122060858A
The invention provides a kit for diagnosing acute myocardial infarction, and belongs to the field of functions and application of genes. The kit comprises a primer pair used for detecting the expression quantity of the NEO-1 gene, a forward primer is SEQ ID NO.1, and a reverse primer is SEQ ID NO.2. By means of the primer pair, the expression quantity of the NEO-1 gene in peripheral blood can be detected, and compared with non-coronary heart disease patients, the expression of NEO-1 in peripheral blood of AMI patients is increased. The expression increase of NEO-1 is found to be an independent risk factor of AMI, and the expression quantity of NEO-1 in peripheral blood of an AMI patient can be used as one of biomarkers of AMI.
Absstract of: CN122060855A
The invention discloses an application of circWHSC1 as a biomarker in preparation of a product for diagnosing or treating ineffective recanalization after ischemic stroke. According to the present invention, the circRNA sequencing results show that the expression of the circWHSC1 (including hsacirc0001388 and nucirc0001336) in the ineffective recanalization patient body is significantly reduced, and the circWHSC1 is verified in the mouse brain tissue, the plasma and the thrombus model of the tMCAO model; functional studies show that the circWHSC1 can significantly reduce the cerebral infarction volume of the mouse. The circWHSC1 can be used for early diagnosis, risk assessment, severity judgment, curative effect monitoring and prognosis judgment of invalid recanalization, and can be used as a drug target for screening candidate drugs for preventing or treating invalid recanalization. The invention provides a molecular diagnosis marker and a therapeutic target for invalid recanalization, and has important clinical value.
Absstract of: CN122060852A
The invention discloses a biomarker and a kit for diagnosing post-stroke depression qi deficiency and blood stasis, liver depression and qi stagnation. The biomarker comprises Clcn3 and/or Nco7. According to the application, by constructing animal models with various diseases and combining ELISA and qPCR technologies, multi-dimensional verification is carried out on candidate targets, and expression changes of the candidate targets in the models are confirmed. Further, by drawing an ROC curve, the diagnostic efficiency (including AUC value, sensitivity and specificity) of each candidate marker is evaluated. Besides, an AAV-mediated RNA interference function experiment is comprehensively applied, a biomarker with diagnosis potential is deeply excavated, and a molecular basis is provided for objective diagnosis of syndromes.
Absstract of: CN122038557A
The invention belongs to the technical field of molecular biology diagnosis and treatment, and relates to application of a reagent for detecting or inhibiting FN1 and a product for diagnosing or preventing and treating vascular restenosis. The expression level of the FN1 in a vascular restenosis sample is remarkably increased, and the FN1 can promote phenotypic transformation of vascular smooth muscle cells (VSMC). Meanwhile, further research proves that the FN1 has better diagnosis efficiency on the diagnosis of the vascular restenosis, and is higher in sensitivity, specificity and accuracy, so that the FN1 can be used for effectively diagnosing the vascular restenosis. In addition, in-vivo experiments prove that VSMC phenotypic transformation can be inhibited and vascular restenosis can be improved by inhibiting FN1 expression. The invention provides a new direction for research and development of vascular restenosis related diagnosis and prevention and treatment products, and has a good clinical application prospect.
Absstract of: CN122031507A
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.
Absstract of: CN122031686A
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.
Absstract of: CN122055460A
Disclosed herein are methods, compositions, and devices for diagnosing and treating diseases, including cardiovascular diseases as well as such diseases and dysfunctions associated with administration of cancer therapy. Methods include sequencing a set of regions in a cell-free nucleic acid molecule and detecting one or more biomarkers indicative of cardiovascular disease and dysfunction.
Absstract of: CN122012735A
The invention discloses a human MTHFR (methylenetetrahydrofolate reductase), MTRR (methylenetetrahydrofolate reductase) and SLC19A1 gene detection kit. The kit is based on a high-resolution melting curve analysis technology, and comprises four groups of primer pairs aiming at C677T and A1298C sites of MTHFR genes, A66G sites of MTRR genes and A80G sites of SLC19A1 genes. The kit can be used for rapidly, sensitively and accurately identifying the genotypes of the four key sites under the same reaction procedure by detecting the melting temperature of PCR products and the difference of curve shapes. The kit is suitable for risk assessment of cardiovascular diseases and birth defects, is more innovatively applied to donor screening and receptor assessment of coprophilous fungus transplantation, fills the blank of genetic background detection tools in the field, and has the advantages of low cost, high sensitivity, high specificity, simplicity and convenience in operation, high repeatability, quick and objective detection result and the like.
Absstract of: CN122012515A
The invention belongs to the technical field of biological medicine and molecular biology, and provides a hypertrophic cardiomyopathy virulence gene MYH7c.794Cgt; the invention relates to T (p.Thr265Ile) and an application thereof. The MYH7 gene mutation is located on the ninth exon, the 794th base is mutated from C to T, namely ACC is mutated to ATC, and the 265th amino acid in the coded amino acid sequence is mutated from threonine to isoleucine. The mutation induces cardiac hypertrophy by disrupting energy metabolism-this defect occurs prior to the occurrence of systolic dysfunction. Along with increasingly prominent status of precision medicine in cardiovascular treatment, a treatment strategy aiming at an upstream pathological process (such as energy homeostasis and mitochondrial dysfunction) provides a way with a wide prospect for preventing and treating MYH7-related hypertrophic cardiomyopathy. MYH7 gene screening has important values in the aspects of promoting early diagnosis, guiding timely treatment intervention and realizing risk-based prevention and management.
Absstract of: CN122012694A
The invention discloses application of ACSS2 as an action target in screening or preparing a medicine for preventing or treating virus-induced vascular remodeling diseases, and belongs to the field of biological medicine. It is found that by inhibiting ACSS2 gene expression or protein activity, Zika virus induced vascular smooth muscle cell phenotypic transformation can be remarkably reversed, and occurrence and development of angiotensin II/aminopropionitrile induced aortic aneurysm/dissection are relieved. The invention provides a siRNA sequence (SEQ ID NO.1-2) specifically targeting ACSS2 and a pharmaceutical composition containing the siRNA, and provides a novel treatment target and a precise intervention tool for virus-related vascular remodeling diseases.
Absstract of: CN122005802A
The invention provides application of an NCOA3 polyQ structural domain in preparation of a medicine for relieving ocular vascular abnormal hyperplasia diseases, relates to the technical field of biomedicine, and aims to solve the problems that in the prior art, an ocular pathological angiogenesis mechanism is complex, and safe and effective targeted intervention means are lacked. The construction of a mouse corneal micropocket pathological angiogenesis model proves that Nco3polyQ structural domain deletion can significantly inhibit corneal neovascularization: compared with a WT mouse, the Nco3wt/Q mouse corneal tissue CD31 positive signal is reduced, the number of corneal neovascularization in the Nco3Q/Q mouse is minimum, and the CD31 positive area is minimum; meanwhile, qPCR (quantitative polymerase chain reaction) detection of corneal tissues shows that mRNA (messenger ribonucleic acid) expression of the vascular marker genes Pecam1 and Cdh5 is in a decreasing trend and is further decreased in an Nco3Q/Q mouse. On the basis, the intervention strategy aiming at the NCOA3 polyQ structural domain is used for preparing the medicine for relieving the abnormal hyperplasia diseases of the ocular blood vessels, and a new treatment strategy and a potential target are provided for related diseases of the ophthalmology department.
Nº publicación: CN121987795A 08/05/2026
Applicant:
XINHUA HOSPITAL AFFILIATED TO SHANGHAI JIAO TONG UNIV SCHOOL OF MEDICINE
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Absstract of: CN121987795A
The invention discloses an application of an IP6K1 gene, an IP6K1 protein and a PAS-A protein fragment in screening and preparing a medicine for preventing and/or treating myocardial infarction diseases or a medicine for improving myocardial cell injury caused by hypoxia. Through research, it is found for the first time that IP6K1 protein is directly combined with a PAS-A substructure domain of HIF-1alpha, and then degradation of the HIF-1alpha, formation of HIF-1alpha/ARNT dimer and combination of the HIF-1alpha and p53 are affected, so that repair of myocardial cell damage caused by hypoxia by the HIF-1alpha is limited, and cell death is aggravated; therefore, the influence caused by myocardial infarction is aggravated. When the IP6K1 gene is knocked out, or the expression of the IP6K1 gene is inhibited, or the IP6K1 protein is degraded, or the expression of a subdomain PAS-A protein fragment of the HIF-1alpha is increased, the combination of the IP6K1 protein and the HIF-1alpha can be eliminated, so that the positive effect of the HIF-1alpha is improved, the repair of myocardial cell injury is improved, the cell survival is promoted, and the adverse influence caused by myocardial infarction is reduced.
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