39 results about "Neointima Formation" patented technology

Restenosis or neointimal formation may occur following angioplasty or other trauma to an artery such as by-pass surgery. This presents a major clinical problem which narrows the artery. The invention provides a balloon catheter with a particular electrode configuration. Also provided is a method whereby vascular cells in the area of the artery subjected to the trauma are subjected to irreversible electroporation which is a non-thermal, non-pharmaceutical method of applying electrical pulses to the cells so that substantially all of the cells in the area are ablated while leaving the structure of the vessel in place and substantially unharmed due to the non-thermal nature of the procedure.

The present invention relates generally to medical devices containing nanoporous surfaces and methods for making same. More specifically, the invention relates to implantable vascular stents or other biomedical devices having at least one nanoporous layer that promotes improved cellular adhesion properties that promote healing and long term biocompatibility. In the case of stents, the nanoporous layer promotes re-endothelialization at sites of stent implantation vasculature, improves overall healing, and reduces inflammation and intimal disease progression. The nanoporous layer may be optionally loaded with one or more therapeutic agent to further improve the function of the implanted stent and further augment clinical efficacy.

Restenosis is inhibited through local delivery of anti-restenotic agents including angiotensin converting enzyme inhibitors; nicotine receptor agonists, agents that increase concentrations of nitric oxide, anti-angiogenic agents, agonists of the TGF-beta receptor; death domain receptor ligands; and thrombin inhibitors. In one embodiment of the invention, the localized delivery is effected through the use of a stent modified for delivery of the agent at the site of injury from balloon angioplasty.

The present invention is related to a low profile endolumenal prosthesis. The prosthesis comprises a radially expandable tubular wire support and an expanded PTFE membrane. The density, wall thickness and intranodal distance of the ePTFE are selected to inhibit the formation and nourishment of a viable neointima on the inner surface of the prosthesis, through the ePTFE membrane.

The present invention relates to the identification of microRNAs that regulate smooth muscle cell proliferation and differentiation, including the miR-143 / miR-145 cluster. Methods of treating restenosis and neointima formation by increasing expression of miR-143 and / or miR-145 are disclosed. The present invention also relates to the identification of two microRNAs, miR-486 and miR-422a, that regulate cell survival in the heart. Methods of treating or preventing cardiac hypertrophy, heart failure, or myocardial infarction by increasing expression of miR-486 and / or miR-422a in heart tissue are also disclosed.

The present invention relates to a composition comprising a bamboo plant extract for the prevention and treatment of inflammatory or blood circulation disease. The extracts of bamboo plant has potent anti-inflammatory activity by inhibiting NO production and blood circulation-improving activity by inhibiting elastase activity and healing the wound of vascular endothelial cell, activating u-PA expression and inhibiting PAI-1 expression, lowering cholesterol deposit and inhibiting neointima formation, therefore it can be used as a therapeutic or health care food for treating and preventing inflammatory or blood circulation diseases.

This invention provides for a method for inhibiting new tissue growth in blood vessels in a subject, wherein the subject experienced blood vessel injury, which comprises administering to the subject a pharmaceutically effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE) so as to inhibit new tissue growth in the subject's blood vessels. The invention also provides for method for inhibiting neointimal formation in blood vessels in a subject, wherein the subject experienced blood vessel injury, which comprises administering to the subject a pharmaceutically effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE) so as to inhibit neointimal formation in the subject's blood vessels. The invention also provides a method for preventing exaggerated restenosis in a diabetic subject which comprises administering to the subject a pharmaceutically effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE) so as to prevent exaggerated restenosis in the subject.

The present invention provides a method of preventing or reducing restenosis, neointima formation, graft failure, atherosclerosis, angiogenesis and / or solid tumour growth in a subject. The method comprises administering to the subject a prophylactically effective dose of a nucleic acid which decreases the level of c-Jun mRNA, c-Jun mRNA translation or nuclear accumulation or activity of c-Jun. It is preferred that the nucleic acid is a DNAzyme that targets c-Jun mRNA.

The present invention relates to a composition comprising a bamboo plant extract for the prevention and treatment of inflammatory or blood circulation disease. The extracts of bamboo plant has potent anti-inflammatory activity by inhibiting NO production and blood circulation-improving activity by inhibiting elastase activity and healing the wound of vascular endothelial cell, activating u-PA expression and inhibiting PAI-1 expression, lowering cholesterol deposit and inhibiting neointima formation, therefore it can be used as a therapeutic or health care food for treating and preventing inflammatory or blood circulation diseases.

The present invention relates to a combination of agents, including an anti-proliferative agent, an anti-inflammatory agent, an anti-growth factor, and an extracellular matrix (ECM) molecule coated on a stent to prevent acute and subacute thrombosis, enhance endothelial in-growth, and prevent neointimal hyperplasia, and / or suppress neovascularization, and thereby reduce restenosis rates for drug eluting stents. The present invention also relates to methods of using such multiple drug eluting stents for the treatment of heart disease and other vascular conditions.

There are provided compounds which can be used in the treatment of diseases mediated by the autophosphorylation of a PDGF receptor, specifically, compounds which can inhibit neointima formation hypertrophy. The compounds are those represented by formula (I) or pharmacologically acceptable salts or solvates thereof: wherein R1 and R2 represent hydrogen, alkyl or the like; R3, R4, R5, and R6 represent hydrogen, halogen, alkyl, alkoxy or the like; R11 and R12 represent hydrogen, alkyl, alkylcarbonyl or the like; and A represents any one of formulae (i) to (x), provided that compounds wherein R3, R4, R5 and R6 represent hydrogen and A represents group (v) wherein u is 0 (zero) and R19 represents phenyl optionally substituted by halogen, alkyl, or alkoxy are excluded.

The present invention provides a method of preventing or reducing restenosis, neointima formation, graft failure, atherosclerosis, angiogenesis and / or solid tumour growth in a subject The method comprises administering to the subject a prophylactically effective dose of a nucleic acid which decreases the level of c-Jun mRNA, c-Jun mRNA translation or nuclear accumulation or activity of c-Jun. It is preferred that the nucleic acid is a DNAzyme that targets c-Jun mRNA.

The present invention is related to a low profile endolumenal prosthesis. The prosthesis comprises a radially expandable tubular wire support and an expanded PTFE membrane. The density, wall thickness and intranodal distance of the ePTFE are selected to inhibit the formation and nourishment of a viable neointima on the inner surface of the prosthesis, through the ePTFE membrane.

Methods for treating or preventing neointima stenosis are disclosed. The methods generally involve the use of a TGFβ inhibitor, a SMAD2 inhibitor, an FGF Receptor agonist, a Let-7 agonist, or a combination thereof, to inhibit endothelial-to-mesenchymal transition (Endo-MT) of vascular endothelial cells into smooth muscle cells (SMC) at sites of endothelial damage. The disclosed methods can therefore be used to prevent or inhibit neointimal stenosis or restenosis, e.g., after angioplasty, vascular graft, or stent. Also disclosed are methods for increasing the patency of biodegradable, synthetic vascular grafts using a composition that inhibits Endo-MT. A cell-free tissue engineered vascular graft (TEVG) produced by this method is also disclosed.

The invention discloses application of brazilin in preparation of products for prevention, mitigation and / or treatment of diseases related to protein tyrosine kinase activity abnormal increase and vascular proliferation. Brazilin has the effects of inhibiting protein tyrosine kinase (PTKs) activity and inhibiting proliferation and migration of the rat thoracic aortic vascular smooth muscle cell (VSMC). Brazilin can prevent, mitigate and / or treat PTKs activity abnormal increase related diseases like tumors, restenosis after percutaneous coronary intervention (PCI), atherosclerosis, high blood pressure, multiple sclerosis, diabetic retinopathy, endometriosis, psoriasis and other skin diseases, asthma and other diseases. Brazilin can prevent, mitigate and / or treat vascular proliferation related diseases like restenosis after PCI, atherosclerosis, high blood pressure, neointima formation after vascular transplantation, vascular diseases after organ transplantation, diabetic angiopathies and the like.

The invention discloses a function and application of an interferon regulatory factor 4 (IRF4) in scaffold and endarterectomy restenosis, belonging to the field of gene functions and applications. According to the application disclosed by the invention, IRF4 gene knockout mice and mild C57 mice are taken as experimental subjects, and a vascular injury model is adopted to carry out neointima formation determination, vascular wall cell proliferation level detection and smooth muscle cell phenotype detection of a vascular injury model mouse; results show that compared with the mild mouse, the IRF4 gene knockout mouse has more distinct neointima formation and cell proliferation, which indicates that the function of the IRF4 gene in scaffold and endarterectomy restenosis is manifested by that the IRF4 gene has effect of inhibiting restenosis caused by vascular injury, especially protecting scaffold and endarterectomy restenosis. As for the function of IRF4, the IRF4 can be used for preparing medicaments for treating angiostenosis, especially medicaments for treating scaffold and endarterectomy restenosis.

The invention discloses an application of immune regulation markers TIPE2 (Tumor Necrosis Factor-a Induced Protein 8 like 2) in preparation of a medicine used for treating vascular proliferation diseases, and also discloses a recombinant adenovirus for expressing the TIPE2. The recombinant adenovirus for the TIPE2 is adopted to realize the in-vivo continuous high expression of TIPE2 protein, which shows the function on inhibiting excess proliferation of a vascular smooth muscle cell, inhibits the hyperplasia of neointima caused by the vascular injury in order to reduce vascular stenting postoperative complication and prognosis and other postoperative complications and prognoses, creates a new path with a wide prospect on effectively preventing and treating the vascular in-stent restenosis of acute coronary syndrome and intervening other vascular proliferation diseases on the cytological basis of vascular smooth muscle proliferation in clinic, and also provides the reference for developing a novel medicine.

The invention discloses functions and application of SHPS1 in treatment of post-vascular injury restenosis, belonging to the field of functions and applications of genes. SHPS1 gene knockout mice and wild type mice are taken as experimental subjects, and due to a vascular injury model, the mouse neointima formation, vascular wall cell proliferation level and smooth muscle cell phenotype transform are detected. The result proves that SHPS1 gene knockout can obviously promote neointima neogenesis and cell proliferation and promote transformation of smooth muscle cells from a shrinkage manner to a synthetic manner. Thus the functions of SHPS1 in post-vascular injury restenosis are realized, which mainly shows that SHPS1 has the functions of inhibiting neointima formation and cell proliferation and inhibiting smooth muscle cell phenotype transformation. Aiming at the functions of the SHPS1, the SHPS1 can be used for preparing medicines and arterial stents for preventing, relieving and / or treating the post-vascular injury restenosis.

Treatments of coronary heart disease including the effect of endothelial shear stress (ESS) on neointimal formation following a bioresorbable vascular scaffold implantation are disclosed.

The present invention relates to a drug eluting device for preventing and treating restenosis and neointimal formation after vascular procedures and / or implantation of implants comprising an implantable or non-implantable device, such as stent, balloon or graft containing an effective amount of at least one retinoid receptors ligand as active ingredient and a coating system.

The invention discloses the function and application of an IRF3 (Interferon Regulatory Factor 3) gene to restenosis after stenting and carotid endarterectomy, belonging to the field of function and application of genes. An IRF3 gene knock-out mouse and a wild C57 mouse are taken as experimental objects, and determination of neointima formation, detection of the vascular wall cell proliferation level and detection of smooth muscle cell phenotype of a blood injury model mouse are performed through the blood injury model. As proved by a result, the neointima formation and cell proliferation of the IRF3 gene knock-out mouse are more remarkable than those of the wild mouse. The function of the IRF3 gene to restenosis after stenting and carotid endarterectomy mainly refers to the function of inhibiting restenosis caused by vascular injury of the IRF3 gene, particularly the function of inhibiting restenosis after stenting and carotid endarterectomy. Aiming at the functions of the IRF3, the IRF3 can be used for preparing medicaments for treating restenosis disease, particularly for preparing medicaments for treating restenosis after stenting and carotid endarterectomy.

Compositions, devices, grafts and methods for reducing or preventing anti-neointima following cardiovascular injuries and interventions are disclosed. The compositions, devices, and grafts typically include an effective amount of a CTP synthase 1 inhibitor to reduce proliferation of vascular smooth muscle cells, without substantial reducing the proliferation of endothelial cells. Methods of reducing neointima formation, accelerating re-endothelialization, and reducing restenosis in a subject using the compositions, devices, and grafts are also disclosed.

The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and / or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.

The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and / or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.

Excessive or repeated activation of inflammatory and pro-coagulant mechanisms at the site of tissue injury contributes to the development scar tissue that can lead to intimal hyperplasia and fibrotic disease. It has been established that inhibition of the LYST protein is associated with reduced inflammatory responses and reduced platelet activation at the site of tissue damage. Compositions and methods for inhibition of the expression and function of the LYST protein are described. The compositions and methods can be useful for the modulation of immune processes that contribute to formation of neointima and fibroproliferative disorders by altering macrophage, platelet and natural killer cell function to create a pro-regenerative immune response.

The present inventions provide various embodiments of methods for one or more of treating vascular injury, neointima proliferation and / or local inflammation in a mammal by locally administering therapeutic compound comprising a mTOR targeting compound and a calcineurin inhibitor. In various aspects, the therapeutic compound comprises a bio-absorbable carrier component carrier component at least partially formed of a cellular uptake inhibitor and a cellular uptake enhancer, a mTOR targeting compound and a calcineurin inhibitor. In various aspects, the present invention provides for controlled delivery, which is at least partially characterized by total and relative amounts of a cellular uptake inhibitor and cellular uptake enhancer in a bio-absorbable carrier component.

Methods for treating or preventing neointima stenosis are disclosed. The methods generally involve the use of a TGFβ inhibitor, a SMAD2 inhibitor, an FGF Receptor agonist, a Let-7 agonist, or a combination thereof, to inhibit endothelial-to-mesenchymal transition (Endo-MT) of vascular endothelial cells into smooth muscle cells (SMC) at sites of endothelial damage. The disclosed methods can therefore be used to prevent or inhibit neointimal stenosis or restenosis, e.g., after angioplasty, vascular graft, or stent. Also disclosed are methods for increasing the patency of biodegradable, synthetic vascular grafts using a composition that inhibits Endo-MT. A cell-free tissue engineered vascular graft (TEVG) produced by this method is also disclosed.

The invention discloses a function and application of an interferon regulatory factor 4 (IRF4) in scaffold and endarterectomy restenosis, belonging to the field of gene functions and applications. According to the application disclosed by the invention, IRF4 gene knockout mice and mild C57 mice are taken as experimental subjects, and a vascular injury model is adopted to carry out neointima formation determination, vascular wall cell proliferation level detection and smooth muscle cell phenotype detection of a vascular injury model mouse; results show that compared with the mild mouse, the IRF4 gene knockout mouse has more distinct neointima formation and cell proliferation, which indicates that the function of the IRF4 gene in scaffold and endarterectomy restenosis is manifested by that the IRF4 gene has effect of inhibiting restenosis caused by vascular injury, especially protecting scaffold and endarterectomy restenosis. As for the function of IRF4, the IRF4 can be used for preparing medicaments for treating angiostenosis, especially medicaments for treating scaffold and endarterectomy restenosis.

The present invention relates to angiotensin I derivatives. In particular, the present invention relates to the use of angiotensin I derivatives, excluding des-aspartate-angiotensin I, for the treatment and / or prevention of cardiac hypertrophy, and / or neointima formation.