7 results about "Cardiac cell" patented technology

The present disclosure provides recombinant adeno-associated virus (rAAV) virions with an engineered capsid protein identified using a high-throughput sequencing screen or rational design. In particular, the disclosure provides AAV5 virions and capsid proteins with increased transduction efficiency in cardiac cells, increased cell-type selectivity, and / or other desirable properties.

A computational system and method for digital modeling of cardiac cell membrane electrophysiology is disclosed. The system generates a digital model representing the cell membrane as a dielectric lipid bilayer comprising a capacitor element and a resistor element, where the resistor element is emulated by a plurality of ion channels. The system calculates cell membrane potential based on intracellular and extracellular concentrations of key ions, such as Na+, K+, Ca2+, and Cl-, using the Goldman-Hodgkin-Katz equation. Generation of cellular membrane action potentials is simulated by modeling the opening and closing of voltage-gated ion channels in response to triggering events. The model provides dynamic visualizations of the distinct phases of the action potential, including depolarization and repolarization, offering a high-fidelity tool for research and for enhancing the realism of training simulations in electrophysiology procedures.

The present disclosure provides recombinant adeno-associated virus (rAAV) virions with an engineered capsid protein. In particular, the disclosure provides AAV9 virions with engineered AAV9 capsid, AAV5 / 9 chimeric capsid or combinatory capsid that achieves increased transduction efficiency in cardiac cells, increased cell-type selectivity, and / or other desirable properties.

The present application relates to a novel micropeptide MP29 and a use thereof and relates to a use of the micropeptide in the preparation of a reagent or drug for preventing, treating, or alleviating diseases related to abnormal mitochondrial energy metabolism in cells, wherein the diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, schizophrenia, aging, photoaging, fatty liver disease, liver fibrosis, liver cirrhosis, liver cancer, diabetic nephropathy, cardiovascular diseases such as heart failure, etc. By means of endogenous overexpression or exogenous synthesis, the reducing equivalents NADH in the tricarboxylic acid cycle are up-regulated to promote intracellular ATP production, thereby significantly enhancing the proliferation of high-energy-demanding cardiac cells and brain tissue cells, or suppressing oxidative damage and apoptosis of cells in Alzheimer's disease models and Parkinsonism, or alleviating hypertrophy and aging of myocardial cells in heart failure models, or ameliorating the photodamage of cells in photoaging models. These results indicate that the micropeptide MP29 has an application value in preventing or treating diseases related to abnormal mitochondrial energy metabolism.

Provided herein are composition and methods for gene therapy of LEM domain-containing protein 2 (LEMD2) cardiomyopathy. Viral vectors are used to deliver LEMD2 reading frame for gene augmentation in cardiac cells that harbor loss-of-function LEMD2 mutations. A murine model for LEMD2 cardiomyopathy is also described.

The present invention provides a heart tissue model of at least 60% cardiac cells, wherein the cardiac cells surround an inner cavity, wherein the cardiac cells are selected from cardiomyocytes, endocardial cells and epicardial cells; method for the generation of such a tissue model and uses thereof.

A method of increasing sodium current in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription, thereby increasing sodium current in the cardiac cell. A method of increasing translation of SCN5A mRNA in a cell generally includes introducing into the cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of decreasing arrythmia in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of treating arrythmia in a patient having, or at risk of having, arrythmia generally includes administering to the patient an miR-448 inhibitor in an amount effective to decrease the likelihood or extent of arrythmia in the patient. In some embodiments of all methods, the miR-448 inhibitor can be an miR-448 antagomir or an miR-448 sponge.