Abstract: The disclosure relates to novel uses and methods for preventing and/or treating heart disease, which employ a therapeutically effective amount of an ActRII receptor antagonist, e.g., an ActRII receptor binding molecule, e.g., an ActRII receptor antibody, such as the bimagrumab antibody.

Abstract: The disclosure provides compositions comprising an inhibitory nucleic acid targeting IncExACTI, and methods of use thereof to improve cardiac function in a subject in need thereof. Specifically, the disclosure provides a cardiac long noncoding RNA (IncRNA), referred as IncExACT 1 (SEQ ID NO: 1), and inhibitory nucleic acids targeting IncExACT 1 for reducing expression of IncExACT 1 and/or Dachsous cadherin-related 2 (DCHS2) in a cell, e.g., a cell in a subject for improving cardiac function in a subject, wherein the subject has pathological cardiac hypertrophy and/or heart failure.

Abstract: The disclosure relates to novel uses and methods for preventing and/or treating heart disease, which employ a therapeutically effective amount of an ActRII receptor antagonist, e.g., an ActRII receptor binding molecule, e.g., an ActRII receptor antibody, such as the bimagrumab antibody.

Abstract: The disclosure relates to novel uses and methods for preventing and/or treating heart disease, which employ a therapeutically effective amount of an ActRII receptor antagonist, e.g., an ActRII receptor binding molecule, e.g., an ActRII receptor antibody, such as the bimagrumab antibody.

Abstract: The invention relates to the use of a CITED4 polypeptide and/or a microRNA-222 or precursor (e.g., pre-miR-222) or mimic thereof, for treating a cardiovascular disease or pathological condition, such as heart failure, myocardial infarction, and for promoting post-myocardial infarction cardiac remodeling in heart tissue.

Abstract: The present invention relates to the treatment of acquired and genetic heart conditions in a subject by the inhibition of SGK1, including Long QT syndrome and cardiovascular disease, including dilated cardiomyopathy. Cardiovascular diseases treatable by SGK1 inhibition include heart failure, arrhythmia, ischemic injury, ischemic infarction, cardiac fibrosis, vascular proliferation, restenosis, dilated cardiomyopathy, and stent failure. The present invention also identifies selective inhibitors of SGK1. The method comprises administering to the subject a therapeutically effective amount of an inhibitor of SG.

Abstract: The disclosure relates to novel uses and methods for preventing and/or treating heart disease, which employ a therapeutically effective amount of an ActRII receptor antagonist, e.g., an ActRII receptor binding molecule, e.g., an ActRII receptor antibody, such as the bimagrumab antibody.

Abstract: The present invention relates to the treatment of acquired and genetic heart conditions in a subject by the inhibition of SGK1, including Long QT syndrome and cardiovascular disease, including dilated cardiomyopathy. Cardiovascular diseases treatable by SGK1 inhibition include heart failure, arrhythmia, ischemic injury, ischemic infarction, cardiac fibrosis, vascular proliferation, restenosis, dilated cardiomyopathy, and stent failure. The present invention also identifies selective inhibitors of SGK1. The method comprises administering to the subject a therapeutically effective amount of an inhibitor of SG.

Abstract: The present invention relates to the treatment of acquired and genetic heart conditions in a subject by the inhibition of SGK1, including Long QT syndrome and cardiovascular disease, including dilated cardiomyopathy. Cardiovascular diseases treatable by SGK1 inhibition include heart failure, arrhythmia, ischemic injury, ischemic infarction, cardiac fibrosis, vascular proliferation, restenosis, dilated cardiomyopathy, and stent failure. The present invention also identifies selective inhibitors of SGK1. The method comprises administering to the subject a therapeutically effective amount of an inhibitor of SG.

Abstract: The present invention relates to the treatment of acquired and genetic heart conditions in a subject by the inhibition of SGK1, including Long QT syndrome and cardiovascular disease, including dilated cardiomyopathy. Cardiovascular diseases treatable by SGK1 inhibition include heart failure, arrhythmia, ischemic injury, ischemic infarction, cardiac fibrosis, vascular proliferation, restenosis, dilated cardiomyopathy, and stent failure. The present invention also identifies selective inhibitors of SGK1. The method comprises administering to the subject a therapeutically effective amount of an inhibitor of SG.

Abstract: The invention relates to the use of a CITED4 polypeptide and/or a microRNA-222 or precursor (e.g., pre-miR-222) or mimic thereof, for treating a cardiovascular disease or pathological condition, such as heart failure, myocardial infarction, and for promoting post-myocardial infarction cardiac remodeling in heart tissue.

Abstract: The present invention relates to the treatment of acquired and genetic heart conditions in a subject by the inhibition of SGK1, including Long QT syndrome and cardiovascular disease, including dilated cardiomyopathy. Cardiovascular diseases treatable by SGK1 inhibition include heart failure, arrhythmia, ischemic injury, ischemic infarction, cardiac fibrosis, vascular proliferation, restenosis, dilated cardiomyopathy, and stent failure. The present invention also identifies selective inhibitors of SGK1. The method comprises administering to the subject a therapeutically effective amount of an inhibitor of SG.

Abstract: A method is described for diagnosing individuals as having hypertrophic cardiomyopathy, e.g. familial or sporadic hypertrophic cardiomyopathy. The method provides a useful diagnostic tool which becomes particularly important when testing asymptomatic individuals suspected of having the disease. Symptomatic individuals have a much better chance of being diagnosed properly by a physician. Asymptomatic individuals from families having a history of familial hypertrophic cardiomyopathy may be selectively screened using the method of this invention allowing for a diagnosis prior to the appearance of any symptoms. Individuals having the mutation responsible for the disease may be counseled to take steps which hopefully would prolong their life, i.e. avoid rigorous exercise. The methodology used in the above method also has broad applicability and may be used to detect other disease-associated mutations in DNA obtained from subject being tested for other disease-associated mutations.

Abstract: A method is described for diagnosing individuals as having hypertrophic cardiomyopathy, e.g. familial or sporadic hypertrophic cardiomyopathy. The method provides a useful diagnostic tool which becomes particularly important when testing asymptomatic individuals suspected of having the disease. Symptomatic individuals have a much better chance of being diagnosed properly by a physician. Asymptomatic individuals from families having a history of familial hypertrophic cardiomyopathy may be selectively screened using the method of this invention allowing for a diagnosis prior to the appearance of any symptoms. Individuals having the mutation responsible for the disease may be counseled to take steps which hopefully would prolong their life, i.e. avoid rigorous exercise. The methodology used in the above method also has broad applicability and may be used to detect other disease-associated mutations in DNA obtained from subject being tested for other disease-associated mutations.

Abstract: The present invention relates to methods for treating or preventing cardiac disorders such as heart failure, by administering to a mammal a therapeutically effective amount of an FADD inhibitor. According to the present invention, the FADD inhibitor is anti-apoptotic, anti-inflammatory, or both. Also disclosed are screening methods that make use of FADD for the identification of novel therapeutics for treating or preventing cardiac disorders.

Abstract: Heart cells in a subject can be treated, for example, by introducing, into the heart of the subject, an adeno-associated virus subtype 6 (AAV6) viral delivery system that includes a functional nucleic acid. For example, the functional nucleic acid encodes a non-viral therapeutic protein, thereby treating the subject.

Abstract: A method for lessening or preventing non-pulmonary ischemia-reperfusion injury or inflammation in a mammal by identifying a mammal which has ischemia-reperfusion or is at risk for developing ischemia-reperfusion in a non-pulmonary tissue; and causing the mammal to inhale a therapeutically effective amount of gaseous nitric oxide sufficient to diminish the ability of leukocytes or platelets to become activated in a manner that contributes to an inflammatory process at the site of the ischemia-reperfusion or inflammation in the non-pulmonary tissue, thereby lessening or preventing non-pulmonary ischemia-reperfusion injury in the mammal.

Abstract: A method is described for diagnosing individuals as having hypertrophic cardiomyopathy, e.g. familial or sporadic hypertrophic cardiomyopathy. The method provides a useful diagnostic tool which becomes particularly important when testing asymptomatic individuals suspected of having the disease. Symptomatic individuals have a much better chance of being diagnosed properly by a physician. Asymptomatic individuals from families having a history of familial hypertrophic cardiomyopathy may be selectively screened using the method of this invention allowing for a diagnosis prior to the appearance of any symptoms. Individuals having the mutation responsible for the disease may be counseled to take steps which hopefully would prolong their life, i.e. avoid rigorous exercise. The methodology used in the above method also has broad applicability and may be used to detect other disease-associated mutations in DNA obtained from subject being tested for other disease-associated mutations.

Abstract: A method for lessening or preventing non-pulmonary ischemia-reperfusion injury or inflammation in a mammal by identifying a mammal which has ischemia-reperfusion or is at risk for developing ischemia-reperfusion in a non-pulmonary tissue; and causing the mammal to inhale a therapeutically effective amount of gaseous nitric oxide sufficient to diminish the ability of leukocytes or platelets to become activated in a manner that contributes to an inflammatory process at the site of the ischemia-reperfusion or inflammation in the non-pulmonary tissue, thereby lessening or preventing non-pulmonary ischemia-reperfusion injury in the mammal.

Abstract: The present invention relates to methods and compositions for reducing or preventing ischemia-reperfusion injury. Methods for identifying candidate compounds for such treatment are also described.