160 results about "Cardiac fibrosis" patented technology

The invention provides a synthetic polypeptide of Formula I′:

The present invention relates to treating or preventing age-related cardiomyopathy by modulating the expression or activity of a miR-34 family member and/or PNUTS. Methods of treating or preventing age-related cardiomyopathy include administering an inhibitor of miR-34 expression or activity or an agonist of PNUTS expression or activity. Also provided herein are methods of treating or preventing cardiac fibrosis and myocardial infarction by administering an inhibitor of miR-34 expression or activity or an agonist of PNUTS expression or activity.

The invention provides a synthetic polypeptide of Formula I′ (SEQ ID NO: 1):

X1-X2-X3-R—X5-X6-X7-X8-X9-X10-X11-X12-X13  I

• • or an amide, an ester or a salt thereof, wherein X1, X2, X3, X5, X6, X7, X8, X9, X10, X11, X12 and X13 are defined herein. The polypeptides are agonist of the APJ receptor. The invention also relates to a method for manufacturing the polypeptides of the invention, and its therapeutic uses such as treatment or prevention of acute decompensated heart failure (ADHF), chronic heart failure, pulmonary hypertension, atrial fibrillation, Brugada syndrome, ventricular tachycardia, atherosclerosis, hypertension, restenosis, ischemic cardiovascular diseases, cardiomyopathy, cardiac fibrosis, arrhythmia, water retention, diabetes (including gestational diabetes), obesity, peripheral arterial disease, cerebrovascular accidents, transient ischemic attacks, traumatic brain injuries, amyotrophic lateral sclerosis, burn injuries (including sunburn) and preeclampsia. The present invention further provides a combination of pharmacologically active agents and a pharmaceutical composition.

A method for treating cardiac fibrosis resulting from injury of a mammalian heart is described comprising the step of contacting a therapeutically effective amount of relaxin and/or an LGR7 activating agent with cardiac cells following the injury in an amount sufficient to reduce the fibrosis. Also described are methods for protecting the heart following an ischemic event, inhibiting the proliferation of activated fibroblasts and antagonising collagen secretion or deposition in a mammalian heart.

The present invention is directed to methods of treating, preventing, and/or ameliorating fibrosis syndrome, and in particular cardiac fibrosis, by administration of a therapeutically effective amount of ifetroban, or a pharmaceutically acceptable salt thereof.

A composition for repressing transformation growth factor β contains theanine as an active substance. The composition is useful for preventing or treating chronic glomerulonephritis, renal interstitial fibrosis, hepatic fibrosis, hepatic cirrhosis, idiopathic interstitial pneumonia, keloid, hidebound disease, arterial sclerosis, myocardial infarction, cardiac fibrosis, restenosis, acute megakaryoblastic leukemia, adult T-cell leukemia, chronic fatigue syndrome or ordinary fatigue.

Endoglin has now been shown to be an important target of therapy to reduce disease symptoms associated with heart failure, particularly cardiac fibrosis. Soluble Endoglin is identified as an anatogonist to TGFβ1 activity, while membrane-bound Endoglin is identified as a necessary component to promote TGFβ1 activity in heart failure. The present invention therefore features methods and kits for treatment of subject having heart failure or a related disorder by administering a composition that decreases TGFβ1 signaling through either direct inhibition of membrane-bound Endoglin or promoting expression of soluble Endoglin.

The invention provides a cyclic polypeptide of Formula I (SEQ ID NO: 1):

X1-R-X3-X4-L-S-X7-X8-X9-X10-X11-X12-X13  I

or an amide, an ester or a salt thereof, or a bioconjugate thereof, wherein X1, X3, X4, X7, X8, X9, X10, X11, X12 and X13 are defined herein. The polypeptides are agonist of the APJ receptor. The invention also relates to a method for manufacturing the polypeptides of the invention or bioconjugates thereof, and their therapeutic uses such as treatment or prevention of acute decompensated heart failure (ADHF), chronic heart failure, pulmonary hypertension, atrial fibrillation, Brugada syndrome, ventricular tachycardia, atherosclerosis, hypertension, restenosis, ischemic cardiovascular diseases, cardiomyopathy, cardiac fibrosis, arrhythmia, water retention, diabetes (including gestational diabetes), obesity, peripheral arterial disease, cerebrovascular accidents, transient ischemic attacks, traumatic brain injuries, amyotrophic lateral sclerosis, burn injuries (including sunburn) and preeclampsia. The present invention further provides a combination of pharmacologically active agents and a pharmaceutical composition.

The invention discloses circRNA CHIF nucleotide and a pharmaceutical composition comprising the circRNA CHIF nucleotide. The pharmaceutical composition comprises the circRNA CHIF nucleotide, an auxiliary, and a viral vector or an embedding vector, the embedding vector is cholesterol, nanoparticles or lipidosome, preferably lipidosome, the viral vector is one or more of adenovirus vector, lentiviral vector and retroviral vector, preferably adenovirus vector, and the auxiliary is one or more of mannitol, phosphate buffer solution and normal saline, preferably phosphate buffer solution, the circRNA MNCR viral vector is 1016 PFU in infectivity titer, and a mass ratio of the circRNA CHIF nucleotide to the lipidosome is 1:1.25; a mass ratio of the viral vector or embedding vector to the auxiliaries is 1:200. The pharmaceutical composition is used for preventing and treating cardiac hypertrophy, cardiac fibrosis, coronary heart disease and heart failure, has reasonable formula, is simple to manufacture, has significant therapeutic effect, is widely applicable and is friendly to service environments.

The invention discloses RNA and application of RNA in diseases of a cardiovascular system. According to RNA, the nucleotide sequence of RNA is a sequence 3 in a sequence table. The invention further provides a gene,encoding RNA. The nucleotide sequence of the gene of RNA is a sequence 4 in the sequence table. The experiment of the invention shows that RNA and the application of RNA in the diseases of the cardiovascular system find that by an induction of isoproterenol (ISO), RNAi method Knock down IHP-55 is used in neonatal rat cardiac fibroblasts to obviously promote proliferation of cardiac fibroblasts; ISO induced activation and kinase activity of P38MAPK can be enhanced in the Knock-down HIP-55 cardiac fibroblasts; and HIP-55 is a new protein which has a protective effect on cardiac fibrosis, and provides a new target for clinical diagnosis, treatment and new medicament development.

Hepatic cirrhosis is considered a severe health problem in Mexico, since it is the third mortality cause in working-age people and there is no 100% effective treatment. Cirrhosis is characterized by an exacerbated increase of collagen in liver parenchyma, replacing the hepatocytes and thus provoking liver failure. This is one of the reasons why we have used a gene therapy through specific delivery to cirrhotic livers of the gene of human urokinase plasminogen activator (huPA), which activates mechanisms that induce the degradation of excess cellular matrix and stimulate hepatocyte proliferation, obtaining thus a fast re-establishment of the liver function. In the instant invention, the modified human uPA gene was inserted in the adenoviral vector (pAd-DeltahuPA), because it is not secreted and does not provoke hypercoagulation or spontaneous internal bleedings. Moreover, data from the bio-distribution essay with an adenoviral vector with reporter gene beta-gal have shown liver specificity as the target organ of the vector. Using ELISA, huPa protein was detected in liver homogenates (4500 pg/ml) in animals treated with pAd-DeltahuPA and was also intracellularly detected through immunochemistry in liver cuts (80% positive cells). huPa induced a dramatic fibrosis reduction (85%) on day 10 of vector administration, compared to control cirrhotic rats and 55% hepatocyte proliferation increase. Liver function tests (ALT, AST, alkaline phosphatase and bilirubin) dropped to nearly normal levels and hepatocyte proliferation was observed. Because of the two beneficial event cascades, gene therapy with modified huPA can be developed as a definite potential treatment for patients with liver cirrhosis.

The invention discloses a function and application of ubiquitin-specific protease 18 (USP18) on treatment of cardiac hypertrophy, and belongs to the field of functions and application of genes. A mutual relation between USP18 expression and the cardiac hypertrophy is determined, and a research result shows that in a model suffering from the cardiac hypertrophy, USP18 expression is obviously lower than that of a normal group; and cardiac hypertrophy and fibrosis are promoted and a cardiac function is worsened by inhibiting USP18 expression, and cardiac hypertrophy and fibrosis are obviously inhibited and the cardiac function is protected by promoting USP18 overexpression. Therefore, the USP18 can serve as a target gene, is used for screening medicines for protecting the cardiac function, resisting cardiac fibrosis and/or preventing and relieving and/or treating cardiac hypertrophy, and is used for preparing medicines for protecting the cardiac function, resisting cardiac hypertrophy and/or preventing and relieving and/or treating cardiac hypertrophy, and a new effective path is provided for treatment of cardiac hypertrophy cardiac hypertrophy.

The invention discloses a function and application of ubiquitin specific protease 4 (USP4) in treating cardiac hypertrophy, and belongs to the field of gene functions and application. The mutual relation between the expression of the USP4 and cardiac hypertrophy is determined; research results show that in a cardiac hypertrophy occurrence model, the expression of the USP4 is significantly reduced compared with a normal group; by restraining the expression of the USP4, the cardiac hypertrophy and fibrosis are significantly promoted, and the cardiac function is deteriorated; by promoting the expression of the USP4, cardiac hypertrophy and fibrosis are significantly restrained, and the cardiac function is protected. Accordingly, the USP4 can be used as a target gene for screening and preparing the medicine which protects the cardiac function, resists cardiac fibrosis and/or prevents, relieves and/or treats cardiac hypertrophy, and an effective new way is provided for treating cardiac hypertrophy.