Patent application number | Description | Published |
20090087412 | Methods and compositions relating to HDAC 4 and 5 regulation of cardiac gene expression - The present invention relates to cardiac hypertrophy. More particularly, the present invention defines the molecular events linking calcium stimulation to cardiac hypertrophy. More specifically, the present invention shows that Ca | 04-02-2009 |
20100212036 | SELECTIVE INHIBITION OF HISTONE DEACETYLASES 1 AND 2 AS A TREATMENT FOR CARDIAC HYPERTROPHY - The present invention provides for methods of treating and preventing cardiac hypertrophy. Class I HDACs, which are known to participate in regulation of chromatin structure and gene expression, have generally been considered as pro-hypertrophic in their action. However, the present invention demonstrates that inhibition of certain Class I HDACs should be avoided in the treatment of cardiac hypertrophy, thereby pointing toward selective, and not global, inhibition of Class I HDACs. In particular, the present invention provides for selective inhibition of HDACs 1 and/or 2, and the avoidance of inhibition of HDAC3. | 08-19-2010 |
20110196017 | MICRO-RNA THAT PROMOTES VASCULAR INTEGRITY AND USES THEREOF - The present invention relates to the identification of a microRNA, designated miR-126, that is a regulator of vascular integrity in endothelial cells. This endothelial cell-restricted microRNA mediates developmental angiogenesis in vivo, and targeted deletion of miR-126 in mice causes leaky vessels, hemorrhaging, and partial embryonic lethality, due to a loss of vascular integrity and defects in endothelial cell proliferation, migration, and angiogenesis. These vascular abnormalities resemble the consequences of diminished signaling by angiogenic growth factors, such as VEGF and FGF. These findings have important therapeutic implications for a variety of disorders involving abnormal angiogenesis and vascular leakage. Methods of treating disease states characterized by ischemia, vascular damage, and pathologic neovascularization by modulating miR-126 function are disclosed. | 08-11-2011 |
20120029200 | Stem Cell Differentiating Agents and Uses Therefor - The present invention relates to screens for compounds that can induce stem cell differentiation. In addition, isoxazoles and sulfonyl hydrazones are identified as general classes of compounds that can induce differentiation of stem cells into cells of neuronal and cardiac fate, respectively. | 02-02-2012 |
20120213738 | Cardiac Repair By Reprogramming of Cardiac Fibroblasts Into Cardiomyocytes - The present invention involves the use of transcription factors including Tbx5, Mef2C, Hand2, myocardin and Gata4 to reprogram cardiac fibroblasts into cardiomyocytes, both in vitro and in vivo. Such methods find particular use in the treatment of patients post-myocardial infarction to prevent or limit scarring and to promote myocardial repair. | 08-23-2012 |
20130005658 | MICRO-RNA REGULATION IN ISCHEMIA AND ISCHEMIA-REPERFUSION INJURY - The present invention relates to the identification of miRNAs that are involved in cardiac remodeling following ischemia and ischemia reperfusion injury. A subset of these miRNAs are regulated in the short term following an ischemic event indicating that these miRNAs play an important role in the induction of subsequent pathological events. Modulation of these identified miRNAs as a treatment or prevention for myocardial ischemia and ischemia reperfusion injury is described. | 01-03-2013 |
20130143935 | STEM CELL DIFFERENTIATING AGENTS AND USES THEREFOR - The present invention relates to screens for compounds that can induce stem cell differentiation. In addition, isoxazoles and sulfonyl hydrazones are identified as general classes of compounds that can induce differentiation of stem cells into cells of neuronal and cardiac fate, respectively. | 06-06-2013 |
20130150427 | REGULATION OF METABOLISM BY MIR-378 - The present invention provides a method of regulating fatty acid metabolism in a cell by contacting the cell with a modulator of miR-378 and/or miR-378* activity or expression. The present invention also provides a method of treating or preventing a metabolic disorder, such as obesity, diabetes, or metabolic syndrome, in a subject by administering to the subject an inhibitor of miR-378 and/or miR-378* expression or activity. Methods of treating or preventing pathologic cardiac hypertrophy, cardiac remodeling, myocardial infarction, or heart failure in a subject by inhibiting the expression or activity of miR-378 and/or miR-378* in a subject are also disclosed. | 06-13-2013 |
20130195891 | Micro-RNA family that Modulates Fibrosis and Uses Thereof - The present invention relates to the identification of a microRNA family, designated miR-29a-c, that is a key regulator of fibrosis in cardiac tissue. The inventors show that members of the miR-29 family are down-regulated in the heart tissue in response to stress, and are up-regulated in heart tissue of mice that are resistant to both stress and fibrosis. Also provided are methods of modulating expression and activity of the miR-29 family of miRNAs as a treatment for fibrotic disease, including cardiac hypertrophy, skeletal muscle fibrosis other fibrosis related diseases and collagen loss-related disease. | 08-01-2013 |
20130245092 | MICRO-RNAS THAT CONTROL MYOSIN EXPRESSION AND MYOFIBER IDENTITY - The present invention relates to the identification of two microRNAs, miR-499 and miR-208b, that repress fast skeletal muscle contractile protein genes. Expression of miR-499 and/or miR-208b can be used to repress fast fiber genes and activate slow fiber genes in the treatment of musculoskeletal disorders. Inhibition of miR-499 and/or miR-208b is proposed as a treatment for cardiac hypertrophy, myocardial infarction, and/or heart failure. Pharmaceutical compositions comprising antagonists and agonists of miR-499 and miR-208b function are also disclosed. | 09-19-2013 |
20130259908 | Micro-RNA Family that Modulates Fibrosis and Uses Thereof - The present invention relates to the identification of a microRNA family, designated miR-29a-c, that is a key regulator of fibrosis in cardiac tissue. The inventors show that members of the miR-29 family are down-regulated in the heart tissue in response to stress, and are up-regulated in heart tissue of mice that are resistant to both stress and fibrosis. Also provided are methods of modulating expression and activity of the miR-29 family of miRNAs as a treatment for fibrotic disease, including cardiac hypertrophy, skeletal muscle fibrosis other fibrosis related diseases and collagen loss-related disease. | 10-03-2013 |
20130261169 | Micro-RNA Family That Modulates Fibrosis and Uses Thereof - The present invention relates to the identification of a microRNA family, designated miR-29a-c, that is a key regulator of fibrosis in cardiac tissue. The inventors show that members of the miR-29 family are down-regulated in the heart tissue in response to stress, and are up-regulated in heart tissue of mice that are resistant to both stress and fibrosis. Also provided are methods of modulating expression and activity of the miR-29 family of miRNAs as a treatment for fibrotic disease, including cardiac hypertrophy, skeletal muscle fibrosis other fibrosis related diseases and collagen loss-related disease. | 10-03-2013 |
20140011859 | ANTIMIR-451 FOR THE TREATMENT OF POLYCYTHEMIAS - The present invention provides methods of treating diseases and disorders associated with aberrant erythropoiesis. Specifically, the present invention provides a method for treating polycythemia in a subject by administering an inhibitor of miR-451. Methods of increasing red blood cell count and treating anemia in a subject by administering miR-451 mimetics are also disclosed. | 01-09-2014 |
20140051745 | MICRO-RNAS OF THE MIR-15 FAMILY MODULATE CARDIOMYOCYTE SURVIVAL AND CARDIAC REPAIR - A family of microRNAs, called the miR-15 family, which includes miR-195, are shown to be up-regulated during pathological cardiac remodeling and repress the expression of mRNAs required for cell proliferation and survival, with consequent loss of cardiomyocytes. Strategies to block expression of the miR-15 family in the heart as a treatment for diverse cardiac disease are provided. | 02-20-2014 |
20140179764 | DUAL TARGETING OF MIR-208 AND MIR-499 IN THE TREATMENT OF CARDIAC DISORDERS - The present invention provides a method of treating or preventing cardiac disorders in a subject in need thereof by inhibiting the expression or function of both miR-499 and miR-208 in the heart cells of the subject. In particular, specific protocols for administering inhibitors of the two miRNAs that achieve efficient, long-term suppression are disclosed. In addition, the invention provides a method for treating or preventing musculoskeletal disorders in a subject in need thereof by increasing the expression or activity of both miR-208 and miR-499 in skeletal muscle cells of the subject. | 06-26-2014 |
20140221464 | Compositions and Methods for Treating Skeletal Myopathy - The present invention provides a method of preventing or treating a myopathy, such as a skeletal myopathy, comprising administering a modulator of a miRNA. In one embodiment, the skeletal myopathy is centronuclear myopathy. The modulator can be an agonist that promotes the expression, function or activity of a miR-133 family member. The miR-133 family member can be miR-133a or miR-133b. | 08-07-2014 |