The invention relates to a method of treating a cardiovascular disease, such as heart failure, in a subject in need comprising the step of administering an inhibitor of bZIP repressor or an activator of p38 or a combination thereof to a subject in need thereby treating the cardiovascular disease. The inhibitor to bZIP repressor is: an inhibitor of ATF3; an inhibitor of JDP2; a co-inhibitor to both ATF3 and JDP2; or a combination of an inhibitor of ATF3 and an inhibitor of JDP2.

An object of the present invention is to provide a novel method for sorting cardiomyocytes. Another object of the present invention is to provide a method for producing high-purity cardiomyocytes and a kit used therefor. The present invention provides a method for sorting cardiomyocytes, comprising a step of introducing miRNA-responsive mRNA into a cell group, wherein the miRNA-responsive mRNA consists of a sequence comprising the following (i) and (ii): (i) a nucleic acid specifically recognized by miRNA specifically expressed in cardiomyocytes, and (ii) a nucleic acid corresponding to the coding region of a gene, wherein translation of (ii) the nucleic acid corresponding to the coding region of a gene into protein is regulated by the nucleic acid sequence in (i) above, thereby achieving the aforementioned objects.

Monocyte-specific nucleic acid aptamers and lipid nanoparticles comprising such for use in drug delivery. Also disclosed herein are use of the aptamer-based lipid nanoparticle drug delivery system for treating heart injury.

The present subject matter provides, inter alia compositions, formulations, and methods for inhibiting, treating, and preventing small vessel diseases.

The technology relates to a method for inducing cardiomyogenesis comprising administering a therapeutically effective amount of either or both of KLF1 and KLF2b to increase the level of KLF1 and/or KLF2b in the cardiomyocytes thereby inducing cardiomyogenesis.

Nucleic acids encoding modified myosin heavy-chain-associated RNA transcripts are provided. The modified myosin heavy-chain-associated RNA transcripts belongs to a cluster of long noncoding RNAs (lncRNA) and bind to chromatin remodeler Brg1 to inhibit Brg1's genomic targeting and gene regulation function. The modified myosin heavy-chain-associated RNA transcripts expressed in an individual inhibit Brg1's gene regulation function and protect the heart of the individual from myopathy and failure. One of the modified heavy-chain-associated RNAs is a 400 base pair fragment segmented from a natural 779 base pair sequence of Mhrt (Mhrt779) and has the same cardioprotective effects as the Mhrt779.

The present invention relates to methods of treating or preventing angiogenesis-related diseases by the administration of stem cells and/or progeny cells thereof.

Non-human animals, and methods and compositions for making and using the same, are provided, wherein said non-human animals comprise a humanization of an Angiopoietin-like protein 8 (ANGPTL8) gene. Said non-human animals may be described, in some embodiments, as having a genetic modification to an endogenous ANGPTL8 locus so that said non-human animals express a human ANGPTL8 polypeptide.

Non-human animals, methods and compositions for making and using the same, are provided, wherein said non-human animals comprise a mutant L-kynurenine hydrolase (or kynureninase) gene. Said non-human animals may be described, in some embodiments, as having a genetic modification in an endogenous kynureninase gene so that said non-human animals express a kynureninase polypeptide that includes an amino acid substitution that results in the elimination of an epitope in said kynureninase polypeptide that is present in the membrane proximal external region of human immunodeficiency virus-1 gp41.

In one aspect, the invention provides methods of inhibiting the effects of MASP-2-dependent complement activation in a living subject. The methods comprise the step of administering, to a subject in need thereof, an amount of a MASP-2 inhibitory agent effective to inhibit MASP-2-dependent complement activation. In some embodiments, the MASP-2 inhibitory agent inhibits cellular injury associated with MASP-2-mediated alternative complement pathway activation, while leaving the classical (C1q-dependent) pathway component of the immune system intact. In another aspect, the invention provides compositions for inhibiting the effects of lectin-dependent complement activation, comprising a therapeutically effective amount of a MASP-2 inhibitory agent and a pharmaceutically acceptable carrier.