7 results about "GATA4" patented technology

The invention discloses application of a composition containing lycium barbarum polysaccharide. The lycium barbarum polysaccharide is used for achieving the effects of resisting aging and removing lipofuscin, particularly, the specific lycium barbarum polysaccharide LBP1C can more remarkably reduce the level of transcription factors GATA4, activate key transcription regulatory factors of autophagy, reduce aging-related secretion phenotypes and inhibit accumulation of lipofuscin, and the lycium barbarum polysaccharide LBP1C has the effects of delaying aging, whitening skin and promoting healthy aging.

The invention relates to cellular microcompartments, each microcompartment successively comprising the following layers, which are organised around at least one lumen: —at least one inner layer of human cells undergoing cardiac differentiation, expressing at least one gene chosen from PDGFRα, MESP-1, NKX2-5, GATA4, MEF2C, TBX20, ISL1 and TBX5, —at least one intermediate layer of isotonic aqueous solution, and—at least one outer hydrogel layer. The invention also relates to the cardiac tissues obtained from said microcompartments and the use thereof, particularly in the treatment of heart disease.

A senescence reprogramming composition and methods of use thereof, kits containing the composition, and their use in tissue repair, tissue regeneration, organ regeneration, reversal of senescence, or any combination thereof. In particular, SOX1, SOX2, SOX3, RCOR2, GMNN, GATA1, GATA2, GATA3, GATA4, GATA6, FOXA2, SOX7, SOX17, NKX3.1, NR5A2, C / EBP alpha, OCT4, PAX1, Klf4, Klf2, GLIS1 and c-MYC are used as inducible factors for reprogramming cells, tissues or organs to a young state. Compositions in the form of engineered nucleic acids, engineered cells, engineered proteins, chemical agents, or any combination thereof are provided for treating disease, preventing disease, modulating tissue repair, modulating tissue regeneration, or any combination thereof.

An aging reprogramming composition, a use method therefor, a kit containing the composition, and the use of the composition in tissue repair, tissue regeneration, organ regeneration, aging reversion, or any combination thereof. The present invention relates to SOX1, SOX2, SOX3, RCOR2, GMNN, GATA1, GATA2, GATA3, GATA4, GATA6, FOXA2, SOX7, SOX17, NKX3.1, NR5A2, C / EBPα, OCT4, PAX1, Klf4, Klf2, GLIS1 and c-MYC, which are used as inducing factors to reprogram cells, tissues or organs to restore a youthful state. Provided is a composition of an activation inducing factor in the form of an engineered nucleic acid, an engineered cell, an engineered protein, a chemical agent, or any combination thereof, wherein the composition is used for treating diseases, preventing diseases, modulating tissue repair, modulating tissue regeneration, or any combination thereof.

The invention discloses an application of an MCP-1 inhibitor in preparation of a medicine for preventing and treating aging-related pathological myocardial hypertrophy, the experiment reveals that MCP-1 is an aging-related pathological myocardial hypertrophy core regulatory factor for the first time, and the MCP-1 is used for up-regulating the protein expression of GATA4, IL-17A, NF-kB-p65 signals, alpha-SMA and Collagen I by activating an IL-17A / MCP-1 / CCR2 / IL-17A signal loop, so that the effect of preventing and treating the aging-related pathological myocardial hypertrophy is achieved. Further, myocardial cell senescence and senescence-related secretory phenotypes, hypertrophy and fibrosis are induced. Experiments prove that the MCP-1 inhibitor can be used for preventing and treating the SA-PCH, can improve the SA-PCH induced by Ang II and / or IL-17A, is free of liver and kidney toxicity and can obviously improve liver and kidney function decline induced by Ang II, and a new way is provided for clinical treatment of the SA-PCH.

The invention discloses a histone H3 hypoacetylation mediated heart gene expression regulation method, and relates to the technical field of biological medicines. Comprising the following steps: inducing a low acetylation state of a specific site of histone H3 in heart tissue by applying a histone acetylation inhibitor so as to inhibit gene expression of embryo transcription factors GATA4 and MEF2C; the low acetylation status is directed against lysine sites of histone H3, including at least one of H3K4, H3K9, and H3K27. The accurate epigenetic regulation and control mechanism is different from the traditional gene knockout or overexpression technology, and the transcriptional activity of the key gene for embryonic heart development is accurately regulated and controlled by regulating histone acetyl under the condition that a DNA sequence is not changed.

The application discloses application of palmitoyltransferase ZDHHC11 in preparation of a drug for treating osteoarthritis. ZDHHC11 catalyzes S-palmitoylation of a substrate APOD by specific binding, and then inhibits a GATA4-P65 signal pathway related to aging, and plays a protective role on aged cartilage cells. Increasing the expression level of Zdhhc11 in vivo helps to regulate extracellular matrix metabolism, inhibit cartilage cell aging, and delay the progression of osteoarthritis. The application first identifies ZDHHC11 as a key palmitoyltransferase, the expression level of which influences cartilage cell aging and osteoarthritis phenotype, and clarifies a downstream molecular mechanism of S-palmitoylation mediated by ZDHHC11 in delaying the progression of osteoarthritis, and verifies that increasing the expression level of Zdhhc11 in vivo can significantly reverse the osteoarthritis phenotype.