89 results about "Myofibroblast" patented technology

The invention belongs to the technical field of biological medicines, and particularly relates to circSamd4 and application thereof in preparation of a medicine for treating myocardial fibrosis. In order to screen and obtain circRNA playing a key role in the myocardial fibrosis process so as to provide a medicine for preparing myocardial fibrosis, the invention provides circSamd4, a vector for reducing circSamd4 expression, a host cell containing the vector and application of the circSamd4 in preparation of the medicine for treating myocardial fibrosis. The circSamd4 which plays a key role in the myocardial fibrosis process is found for the first time, the nucleotide sequence of the circSamd4 is shown as SEQ ID NO: 1 or SEQ ID NO: 2, and it is verified that knocking down circSamd4 expression can improve cardiac systolic function damage caused by thoracic aortic arch constriction for four weeks, relieve myocardial fibrosis, inhibit myocardial fibroblast activation and inhibit myocardial fibrosis. The compound can be used for preparing medicines for treating myocardial fibrosis, and has important practical significance.

A conjugate of the formula (I) wherein F is a ligand (radical thereof) that binds fibroblast activation protein alpha (FAPα); L is a functionalized linker that binds with F, A, and X; A is a pharmacokinetic extender that binds or associates or binds with a protein in the blood of an animal; and X is chelator; a method of imaging cancer-associated fibroblasts (CAFs) and activated myofibroblasts in a subject; and a method of treating a disease characterized by upregulation of FAPα, such as cancer, in a subject.

The invention relates to the technical field of biological medicine, in particular to a composite drug-loaded nano preparation and a preparation method thereof. The composite drug-loaded nano-preparation comprises a drug-loaded nano-liposome, and a biological enzyme and a myofibroblast targeting ligand which are loaded on the surface of the drug-loaded nano-liposome, the drug-loaded nano-liposome is a nano-liposome in which an anti-fibrosis drug is encapsulated; the mass ratio of the drug-loaded nano-liposome to the biological enzyme to the myofibroblast targeting ligand is (6-15): (0.5-4): (0-3). According to the invention, a composite drug-loaded nano preparation for pulmonary drug delivery in an aerosol inhalation manner is constructed, and the myofibroblast targeting ligand and the biological enzyme are jointly modified on the surface of the drug-loaded nano liposome; and the composite nano preparation (CLG-CS-FAP-NIN) which has myofibroblast targeting and can degrade excessive collagen in an extracellular matrix is prepared and is used for treating the pulmonary fibrosis.

The invention discloses a stem cell preparation for treating pulmonary fibrosis. The stem cell preparation is mesenchymal stem cell surface modified nanoparticles. The nanoparticles are ROS (reactive oxygen species) response type lipid polymer hybrid nanoparticles loaded with an anti-fibrosis drug. According to the invention, a hydrophobic drug and a hydrophilic anti-fibrosis drug can be simultaneously loaded through the reductive hybrid nanoparticles, and can be delivered to the lung by utilizing the inflammation targeting capability of stem cells. The polymer in the nanoparticles reacts with active oxygen in the microenvironment to promote drug release, and then the effect of protecting stem cells is achieved. The released medicine can induce dedifferentiation of myofibroblasts and inhibit apoptosis of vascular endothelial cells and endothelial mesenchymal transformation, and the mesenchymal stem cells release growth factors at the same time to promote angiogenesis, reconstruct capillary structures deleted in fibrosis areas, promote lung tissue regeneration and recover lung functions to achieve the effect of treating pulmonary fibrosis.

The invention belongs to the technical field of biological medicine, and particularly relates to application of Serpin1 gene as a target spot in preparation of medicine for preventing or treating myocardial fibrosis. In order to screen key molecules for intervening and regulating extracellular matrix balance and provide a basis for developing drugs for preventing or treating myocardial fibrosis, the important function of Serpin1 in myocardial fibrosis is defined through experiments, and the application of Serpin1 gene as a target in preparation of drugs for preventing or treating myocardial fibrosis is provided. Experiments prove that knocking down Serpin1 expression can improve cardiac systolic function damage caused by constriction of the thoracic aortic arch for four weeks, relieve myocardial fibrosis and inhibit activation of myocardial fibroblasts, can be used for preparing the medicine for preventing or treating myocardial fibrosis, and has important practical significance.

The embodiment of the invention provides a self-powered microneedle patch for repairing hypertrophic scars as well as a preparation method and application of the self-powered microneedle patch. The self-powered microneedle patch comprises: a friction nano-generator for generating a current; the conductive drug-loaded microneedle patch is connected with the friction nano-generator, and the friction nano-generator is connected with the conductive drug-loaded microneedle patch; the conductive drug-loaded microneedle patch comprises a conductive microneedle patch body and a crosslinked gelatin-crosslinked hyaluronic acid microneedle bearing Sb4. The surface of the conductive micro-needle patch is provided with a metal coating, and the conductive micro-needle patch is used for mediating current generated by the friction nano-generator and applying percutaneous electrical stimulation; the cross-linked gelatin-cross-linked hyaluronic acid microneedle is coated at the tip of the conductive microneedle patch. According to the self-powered microneedle patch provided by the embodiment of the invention, myofibroblasts of hypertrophic scars are transdifferentiated into adipocytes by providing percutaneous electrochemical stimulation, inflammatory factor release is inhibited, and a tissue microenvironment is remodeled, so that the hypertrophic scars are reversed, and skin repair and tissue regeneration are realized.

The invention provides a myocardial cell reprogramming method, a related preparation and application. The invention provides a myocardial cell reprogramming method which comprises the following steps: carrying out balling culture on myofibroblasts on bionic interpenetrating network hydrogel, so that the myofibroblasts are gathered, and reprogramming the myofibroblasts into myocardial-like cells. The myofibroblasts used before culture are in an activated state. According to the method for realizing cell reprogramming based on the bionic interpenetrating network hydrogel, cell nucleus transplantation, virus transfection or gene editing are not needed, additional chemical induction reagents are not needed, the safety is high, and the effect is remarkable. And culturing supernate based on the reprogrammed cell balls for treating myocardial fibrosis.

The application discloses a new application of a JAK inhibitor and a medicine for promoting skin stretch regeneration, and application of the JAK inhibitor in preparation of the medicine for promoting skin stretch regeneration; the medicine for promoting skin stretch regeneration comprises the following components: a JAK inhibitor and a carrier, wherein the carrier comprises sodium hyaluronate and propylene glycol; the application provides a new application of the JAK inhibitor, and the JAK inhibitor can promote skin stretch regeneration, in particular, can promote increase of hair follicle density, increase of epidermis thickness, increase of dermis thickness, reduction of fibrosis degree, reduction of immune infiltration degree and reduction of myofibroblast quantity after skin expansion.

The invention provides a lung tissue sustained and controlled release material loaded with BMP4 and GANT61 and a preparation method of the lung tissue sustained and controlled release material, and relates to the technical field of disease treatment and delivery materials. The invention relates to a preparation method of a lung tissue sustained and controlled release material loaded with BMP4 and GANT61. The preparation method comprises the following steps: synthesizing HPG by adopting an anionic ring-opening polymerization method; the preparation method comprises the following steps: mixing HPG with PLA, and reacting to prepare a copolymer PLA-HPG; the copolymer PLA-HPG and GANT61 are blended and subjected to a reaction, and nano particles loaded with GANT61 are prepared; and the GANT61-loaded nano particles and BMP4 are subjected to a mixed reaction, such that the BMP4 and GANT61-loaded lung tissue sustained and controlled release material is prepared. The invention constructs a lung tissue sustained and controlled release material loaded with BMP4 and GANT61, and verifies that the lung tissue sustained and controlled release material can realize an anti-pulmonary fibrosis treatment strategy by inducing alpha-SMA + myofibroblast transdifferentiation, resisting inflammation, resisting oxidation and other multiple targets.

Methods, compositions, and kits of parts for preventing or reducing wound contraction. Methods that may include reducing or eliminating a contractile force applied at a tissue wound site by a continuous myofibroblast network. Compositions may include a biocompatible liquid, and a myofibroblast receptor binding agent dispersed in the biocompatible liquid. Kits of parts may include a reservoir and an applicator, such as a nozzle, needle, brush, dropper, or roller.

This invention discloses a method for preparing a co-loaded dual-gene targeted delivery system and its application, involving the construction and preparation of a dual-gene (pHNF4α, pFOXA3) delivery system. This delivery system can target myofibroblasts (MFs) and activated hepatic stellate cells (aHSCs) and can be used for gene therapy of liver fibrosis. This invention synthesizes the targeting carrier material PEI. 25K -PEG 2K -pPB, through electrostatic adsorption, combines with pHNF4α and pFOXA3 to form a co-loaded dual-gene targeted delivery system, F4α / A3@PP-pPB. This delivery system, through the targeting group pPB, binds to MFs (metacellular matrix cells) that lead to excessive accumulation of extracellular matrix in fibrotic livers and to PDGFR (polydimethylformamide) highly expressed on the surface of aHSCs. On the one hand, it inhibits the activation of aHSCs; on the other hand, it transdifferentiates MFs into hepatocyte-like cells (iHep). These two modes, while combating liver fibrosis, can also achieve a certain degree of liver function reconstruction through transdifferentiated iHep cells, providing new ideas and methods for the effective treatment of liver fibrosis.

The application relates to the field of biomedical technology, and discloses an application of a GCA-NAb monoclonal antibody in the preparation of a drug for preventing and / or treating pulmonary fibrosis. The application mainly relates to the application of an amino acid sequence of the GCA-NAb monoclonal antibody as shown in SEQ ID No. 2 in the preparation of the drug for preventing and / or treating pulmonary fibrosis. The GCA-NAb monoclonal antibody can significantly improve pulmonary fibrosis, and can prolong the survival cycle of a mouse model, reduce the proportion of TH17 cells in lung tissues, and slow down the progress of pulmonary fibrosis. In addition, the antibody can directly affect the transformation of fibroblasts, inhibit the transformation of the fibroblasts into myofibroblasts, and thus reduce the fibrosis. The GCA-NAb monoclonal antibody has the characteristics of high efficiency and safety.

The present invention provides a copolymer which has a hydrophobic constituent unit (a), wherein the polymer terminal is a structure (T) containing a trithiocarbonate structure and a C8-15 hydrocarbon group. The present invention also provides a copolymer which has a constituent unit (b) containing an N-acetylglucosamine group, wherein the polymer terminal is a structure (T) containing a trithiocarbonate structure and a C8-15 hydrocarbon group.

The invention belongs to the technical field of 3D printing, and particularly relates to a low-temperature DLP 3D printing method for low-concentration collagen and application of the low-temperature DLP 3D printing method. The printing performance of the photosensitive collagen ColMA bio-ink can be obviously improved in a pH 3 system for the first time, and the durable high-activity collagen biological scaffold is obtained through low-temperature DLP 3D printing; compared with a high-concentration GelMA scaffold, the low-concentration ColMA biological scaffold has higher mechanical performance, shorter equilibrium swelling time, lower swelling ratio, higher degradation resistance and higher biological activity, can remarkably promote proliferation, adhesion and migration of human prepuce fibroblasts and differentiation of the human prepuce fibroblasts into myofibroblasts, and has the advantages of being capable of remarkably improving the human prepuce fibroblasts in the human prepuce fibroblasts and improving the human prepuce fibroblasts in the human prepuce fibroblasts in the human prepuce fibroblasts in the human prepuce fibroblasts in the human prepuce fibroblasts. The inflammatory response of the rat full-thickness skin injury part is effectively relieved, wound reepithelization and ordered collagen deposition are promoted, full-thickness skin injury regeneration is accelerated, and wide application prospects are achieved in tissue regeneration engineering.

The invention relates to medical application of an asparagine endopeptidase inhibitor in mitral valve mucus-like degeneration, and belongs to the technical field of biological medicine. The invention provides an application of an asparagine endopeptidase inhibitor in preparation of a medicine for treating mitral valve mucus-like degeneration. The invention relates to an application in preparation of a medicine for relieving mitral valve insufficiency. The invention relates to application in preparation of a medicine for inhibiting mitral valve thickening. The invention also discloses an application of the LGMN in preparing a medicine for treating mitral valve mucus-like degeneration by inhibiting the LGMN secreted by the in-situ macrophages. According to the application disclosed by the invention, the LGMN secreted by the macrophages is subjected to targeted antagonism, so that the myofibroblast transformation of the valvular interstitial cells is delayed, and a new target spot and a treatment path are provided for precise treatment of the mitral valve mucus-like degeneration.

A modality for preventing or treating fibrotic diseases by identifying a marker protein for myofibroblasts is provided. The present invention relates to prophylactic or therapeutic agents for fibrotic diseases, which contain an inhibitor of GPR176 as an active ingredient.

The invention relates to the technical field of medicines, in particular to a novel medical application of a phosphodiesterase 4B inhibitor namiklast, and particularly relates to an application of namiklast in preparation of a medicine for treating intervertebral disc fibrosis through targeted inhibition of macrophage-myofibroblast transformation.

The invention belongs to the technical field of anti-adhesion materials in biomedical engineering, and relates to an anti-adhesion membrane with coarse structure fibers and a preparation method of the anti-adhesion membrane. The method comprises the following steps: soaking an electrostatic spinning fiber membrane containing a high polymer material and a hydrophilic anti-adhesion component in a treating fluid containing the high polymer material and consisting of a poor solvent and a good solvent for a specific time, rinsing and drying to obtain the anti-adhesion membrane, the swelling ratio of the high polymer material in the treating fluid at 25 DEG C for 10 minutes is 1-10% due to the proportion of the inferior solvent to the benign solvent in the treating fluid. A stable integrated nano shish-kebab structure is formed on the surface of the prepared anti-adhesion membrane fiber, exogenous drugs are not needed, spreading of fibroblasts is limited by means of a physical topological structure, conversion of the fibroblasts to myofibroblasts is blocked, the anti-adhesion effect is good, and biocompatibility is good.

The invention discloses application of arabinoxylan (AX) in preparation of a medicine for treating chronic obstructive pulmonary disease (COPD), and belongs to the technical field of medicines. The arabinoxylan (AX) can be used for preparing a medicine for treating the COPD (chronic obstructive pulmonary disease). Through a large number of researches, the inventor of the application finds that AX has a remarkable COPD treatment effect: lung inflammation in a mouse COPD model caused by haze can be reduced, the expression is that infiltration of mature T lymphocytes and macrophages in lung tissues is reduced, and the expression level of various proinflammatory factors including TGF-beta1 is reduced; the compound can weaken extracellular matrix deposition in the lung of a COPD mouse caused by haze, reduce the thickness of a tracheal wall, and reduce the expression of I-type collagen (collagen I) and a myofibroblast marker smooth muscle alpha2-actin (alpha-Sma); the emphysema degree of a COPD mouse induced by haze is also relieved; the AX also relieves abnormal changes of related protein levels of iron metabolism, mitochondrial metabolism, oxidative stress and glycometabolism in the lung tissue of the COPD mouse induced by haze. Therefore, AX can be used for preparing the medicine for treating COPD.

The invention provides a biomarker combination for evaluating the progress of abdominal aortic aneurysm based on an adventitia and application of the biomarker combination, and the biomarker combination comprises at least two biomarkers selected from the following three independent groups, the at least two markers are from the same group or different groups: a myofibroblast transformation marker group: alpha-smooth muscle actin, monocyte chemotactic protein 1 and a tissue metalloproteinase inhibitor 1; the lipid metabolism related biomarker group comprises a lipid metabolism related protein CD36, carnitine palmitoyl transferase 1 and a fatty acid binding protein 4; and an inflammatory factor related biomarker group: IL-6, MCP-1 and TIMP1. According to the biological marker combination for evaluating the progress of the abdominal aortic aneurysm based on the adventitia, multi-channel biological markers are systematically integrated, an innovative tool is provided for accurate diagnosis, drug screening and curative effect monitoring of AAA, and meanwhile, an important foundation is laid for developing a collaborative treatment strategy based on adventitia fibroblast regulation.

The invention discloses a targeted exosome loaded with siFKBP10 as well as a preparation method and application of the targeted exosome. The targeted exosome comprises a cell exosome with a membrane protein Lamp2b and a myofibroblast RDYH58 peptide which is combined with the membrane protein, and the cell exosome is modified by the siFKBP10; the cDNA (complementary deoxyribonucleic acid) sequence of the RDYH58 peptide is as shown in SEQ. ID. NO.1; 1, and the positive-sense strand of the siFKBP10 is as shown in SEQ ID NO. 2, and the antisense strand of the siFKBP10 is as shown in SEQ ID NO. 3. The targeting exosome can significantly reduce expression of FKBP10 in cells, inhibits excessive deposition of extracellular matrix, has a good inhibition effect on idiopathic pulmonary fibrosis, and provides a new treatment strategy for treatment of IPF.

The present application relates to the application of delta-Viniferin in the preparation of drugs for preventing or treating metabolic cardiovascular diseases. Delta-Viniferin can inhibit the expression level of aging and inflammation related genes / proteins of vascular endothelial cells, reduce endothelial dysfunction, and clarify its anti-hypertensive effect. Delta-Viniferin can inhibit the expression level of vascular smooth muscle cell phenotype conversion related genes / proteins, improve the contraction function of vascular smooth muscle, and significantly alleviate the degradation of elastic fibers of the vascular wall and the rupture of the intima of the aortic wall in vivo, and clarify its effect on preventing and treating aortic dissection. Delta-Viniferin can inhibit the expression level of myocardial fibroblast fibrosis related genes / proteins, and clarify its anti-myocardial fibrosis effect. Delta-Viniferin can promote white adipose tissue browning by targeting the SIRT1-FOXO1 axis, increase energy consumption, and clarify its effect on resisting obesity. In summary, the compound delta-Viniferin has the effect of protecting various metabolic cardiovascular diseases, and can be used to prepare drugs for preventing and treating metabolic cardiovascular diseases.

The invention relates to the field of binding molecules comprising at least one single variable antibody domain, targeted at receptors present on myofibroblasts and / or hepatic stellate cells (HSCs). The invention also relates to a binding molecule comprising at least two single variable antibody domains, each targeting a receptor on HSCs and / or on myofibroblasts. The invention further relates to nucleic acids encoding such binding molecules, a host cell for expression of such binding molecules and to methods for preparing such binding molecules. The invention further relates to pharmaceutical compositions that comprise such binding molecule and to uses of such binding molecules and / or compositions, in particular for prophylactic, therapeutic or diagnostic purposes.

The invention relates to an application of a succinate dehydrogenase subunit SDHC protein and a coding gene thereof in preparation of a medicine for preventing and / or treating renal fibrosis, and belongs to the field of biological medicines. The invention proposes and verifies that SDHC gene delivery can alleviate kidney pathological changes of chronic kidney diseases for the first time; the expression level of kidney tissue fibrosis related indexes is reduced; the transdifferentiation of renal tubular epithelial cells to myofibroblasts is inhibited. SDHC gene delivery can achieve the effect of improving the chronic kidney disease, and good development and application prospects are achieved.

Provided is the use of an effective amount of alpha-enolase (enolase-1, ENO-1) antagonist in manufacturing a medicament for treating a fibrotic disease. ENO-1 antagonist significantly attenuated body weight loss and lung weight gain as well as the fibrosis lesion and collagen deposition in lungs. Also, ENO-1 antagonist significantly reduced cell migration and secretion of collagen and TGF-β in primary mouse lung myofibroblasts.

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 invention belongs to the field of biological medicines, and particularly discloses application of a beta-carbon alkali alkaloid derivative, i.e., senecionone, in preparation of an anti-pulmonary fibrosis medicine, and a series of experiments prove that the senecionone can regulate and control a TGF-beta / SMAD signal channel by inhibiting phosphorylation of SMAD < 2 / 3 >, so that fibroblasts are inhibited from being converted into myofibroblasts, and the anti-pulmonary fibrosis effect is achieved. The generation of extracellular matrix protein COL1 and the like is reduced, so that the pulmonary fibrosis is relieved.

An antifibrotic agent is provided, including a copolymer having a constitutional unit (a) containing an N-acetylglucosamine group and a constitutional unit (b) containing a structure represented by General Formula (b) (provided that a constitutional unit corresponding to the constitutional unit (a) is excluded). In General Formula (b), Yb represents a divalent linking group including an oxygen atom. Rb represents a hydrogen atom or an organic group. * represents a bonding site.

The application belongs to the technical field of biological medicine, and particularly relates to a use of Serpine1 gene as a target in preparation of a drug for preventing or treating myocardial fibrosis. In order to screen key molecules for intervention and regulation of extracellular matrix balance, and provide a basis for development of a drug for preventing or treating myocardial fibrosis, the application determines important functions of Serpine1 in myocardial fibrosis through experiments, and provides a use of Serpine1 gene as a target in preparation of a drug for preventing or treating myocardial fibrosis. The application verifies through experiments that knocking down expression of Serpine1 can improve impaired cardiac systolic function caused by thoracic aortic arch constriction for 4 weeks, reduce myocardial fibrosis, and inhibit activation of myocardial fibroblasts, and can be used for preparation of a drug for preventing or treating myocardial fibrosis, and has important practical significance.

The application belongs to the technical field of biological medicine, and particularly relates to an application of an expression agonist of lncRNA Morrbid in preparation of a drug for delaying heart failure and a pharmaceutical composition. The application first confirms a protective effect of lncRNA Morrbid in heart failure, proves that the lncRNA can significantly inhibit activation of myocardial fibroblasts and collagen deposition, reveals that the lncRNA is involved in regulation of key fibrosis and inflammatory signal pathways, and provides a new molecular intervention target for heart failure.