11 results about "Cardiac fibroblast" patented technology

The invention belongs to the technical field of biology, and particularly relates to a CFTSR gene, a CFTSR gene simulant and application of the CFTSR gene simulant. The nucleic acid sequence of the CFTSR gene is as shown in SEO ID NO. 1. The nucleic acid sequence of the CFTSR gene simulant is as shown in SEO ID NO. 2. The CFTSR gene provided by the invention can be used as a marker for fibroblast activation, and is used for a kit for detecting cardiac fibroblast activation. The CFTSR gene simulant can be used as a therapeutic drug for myocardial infarction injury, and the overexpression of the CFTSR gene can significantly inhibit the proliferation of fibroblasts and activate the repair of damaged myocardial tissues. Based on CFTSR mimics, a simulant of the CFTSR gene is constructed, and the simulant can be conveyed to the position of a heart lesion and can be used as a medicine for treating myocardial infarction injury, so that effective treatment of the lesion is realized.

A system and method for distinguishing non-failing from failing cardiac fibroblasts (CFs) using advanced imaging techniques and machine learning (ML). The method involves staining CFs with fluorescent dyes to highlight key cellular components, such as nuclei and actin fibers. Images are analyzed to extract morphological features, which are then processed and normalized. A supervised ML system, trained on labeled CF data, classifies CFs based on phenotypic differences. The system enables accurate diagnosis of heart failure (HF), facilitates screening for therapeutic efficacy, and identifies antifibrotic agents by evaluating changes in CF phenotypes pre- and post-treatment.

The invention relates to the field of biological medicine, in particular to a si-RNA composition for inducing cardiac fibroblasts to transdifferentiate into endothelial cells and application of the si-RNA composition. The si-RNA composition comprises a si-RNA (Ribonucleic Acid) aiming at a gene Huwe1, a si-RNA aiming at a gene Ltbp3, a si-RNA aiming at a gene Dysf and a si-RNA aiming at a gene Hivep3. The HLDH (Huwe1, Ltbp3, Dysf and Hive3) combined knockout can be used for successfully inducing the transformation of fibroblasts into endothelial cells in an in-vitro ischemia and hypoxia state. A carrier containing shRNA capable of expressing and generating the si-RNA composition is delivered into the heart, so that cardiac fibroblasts undergo transdifferentiation in vivo and participate in angiogenesis, and therefore, increase of fibrosis area and adverse ventricular remodeling after myocardial ischemia are limited through ways such as fibrosis remodeling, the heart function is retained, and myocardial ischemia is improved and repaired.

Providing gene vector regulation using microRNAs expressed in cardiomyocytes. [Solution] This disclosure provides vectors and methods of using them for cell-type-specific repression of the expression of transgenes (e.g., cardiomyocyte reprogramming factors) using microRNA binding sites. The present invention generally relates to vectors and methods of using them for cell-type-specific repression of the expression of transgenes (e.g., cardiomyocyte reprogramming factors). This disclosure provides vectors comprising microRNA binding sites configured to promote specific repression of the expression of transgenes (e.g., cardiomyocyte reprogramming factors) in cardiomyocytes and cardiomyocyte progenitor cells compared to cardiac fibroblasts.

The invention relates to the field of cell engineering, and particularly discloses a preparation method and application of a conditionally immortalized human myocardial fibroblast model. According to the method, a Tet-on system driven by a cardiac fibroblast specific promoter is constructed to regulate and control a lentiviral vector of an SV40LT-tsA58 temperature-sensitive mutant gene, and after primary human cardiac fibroblasts are transduced, conditional immortalization of the cells is realized in the presence of an inducer doxycycline. The model can be stably amplified under an induction condition, the immortalized gene expression is closed after an inducer is removed, the primary physiological state of cells is recovered, and the high-fidelity response capability to fibrosis promoting and anti-fibrosis drugs is reserved. According to the method, the in-vitro proliferation limit of primary cells is broken through, the problems of species difference and ethics are avoided, and a humanized, high-fidelity and high-controllability standardized tool is provided for myocardial fibrosis pathological mechanism research and drug screening.

The invention discloses application of a composition containing a tanshinone extract and muscone, and belongs to the technical field of medicines. Through compatibility and proportion control of the tanshinone extract and the musk ketone, heart fibroblast expression and / or FSTL1 secretion can be inhibited on the molecular level, related fibrosis signal channels are regulated and controlled, accordingly, the myocardial fibrosis process is inhibited, a synergistic effect with myocardial damage resistance is achieved, ventricular structure and dysfunction after myocardial infarction is improved, and the myocardial infarction treatment effect is improved. The pharmaceutical composition is used for treating cardiovascular diseases such as myocardial infarction, myocardial fibrosis and heart failure after myocardial infarction. The composition disclosed by the invention comprises tanshinone extract and muscone, and can be used for preparing medicines with better effects for preventing and treating cardiovascular diseases.

The invention discloses a 3-aryl coumarin derivative as well as a preparation method and application thereof, and the preparation method comprises the following steps: reacting substituted 2-bromobenzaldehyde with a substituted aryl acetic acid compound to obtain a substituted E-2, 3-diaryl acrylic acid compound; and in the presence of cuprous oxide and potassium carbonate, heating and reacting in N, N-dimethylformamide to obtain the 3-aryl coumarin derivative. The 3-aryl coumarin derivative disclosed by the invention can be combined with BRD4, has remarkable inhibitory activity on the BRD4, has a protective effect on primary myocardial cells caused by ischemia reperfusion, can inhibit proliferation, migration and invasion of cardiac fibroblasts, and can inhibit ferroptosis of hypoxia / reperfusion injury myocardial cells; the compound can be used for preparing medicines for treating diseases related to abnormal BRD4 activity.

The invention relates to the technical field of biological medicine, in particular to a marker for diagnosis and treatment of heart failure and application of the marker, and aims to solve the problem that in the prior art, systematic and deep research on CTHRC1 in a pressure overload model closer to human heart failure pathology is lacked. The application proves that the expression level of the CTHRC1 is obviously up-regulated no matter in heart tissues and serum of an animal model or serum of a clinical sample, so that the reliability and the sensitivity of the CTHRC1 as the heart failure biomarker are proved, and a brand-new diagnostic marker directly related to fibrosis pathology is provided for the heart failure; in addition, it is also clearly proposed that the CTHRC1 monoclonal antibody is used for preparing a medicine for treating heart failure, and the CTHRC1 monoclonal antibody can neutralize and effectively block the specific biological function activity of a CTHRC1 immunogen through high binding affinity, and can become a new treatment target for relieving or reversing cardiac fibroblast activation and cardiac fibrosis.

The disclosure generally relates to methods, cells, and compositions for preparing cardiac extracellular matrix. In particular, provided herein are methods for preparing a cardiac extracellular matrix using SUSD2 High fibroblasts and SUSD2 High myofibroblasts.

The application discloses a kind of myocardial fibrosis organoid model construction methods based on natural toxin induction, belong to biomedical engineering and drug screening technical field.The application aims at solving the problems of existing two-dimensional in vitro model pathological mechanism not true, microenvironment is missing and not friendly to multi-target natural product screening.The model is formed by human pluripotent stem cell-derived cardiomyocytes and cardiac fibroblasts are co-cultured in three-dimensional matrigel according to a certain proportion.The application uses natural toxin that can induce endoplasmic reticulum stress of cardiomyocyte, in a chronic, low-concentration manner stimulates organoid, simulates the gradual fibrosis process initiated by myocardial cell injury, mediated by paracrine signal, to provide a new in vitro drug screening platform with more real pathological mechanism, more complex microenvironment, more suitable for screening natural product with multi-target mechanism.