76 results about "Myofibroblast" patented technology

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 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.

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 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.

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.

The invention discloses a nano preparation for blocking malignant crosstalk of mechanical and biochemical signals of a lung. The preparation is composed of lipid nanoparticles composed of phospholipid, cholesterol and DSPE-PEG2K-NH2, the surfaces of the lipid nanoparticles are grafted with L-arginine and tannic acid, the two drugs are cooperatively loaded, and double intervention on mechanical and biochemical signal channels is achieved. Tannic acid modification can remove active oxygen and enhance lung targeting, and L-arginine is helpful to penetrate through a compact extracellular matrix and promote delivery of drugs to the deep part of pulmonary alveoli. On one hand, by promoting phenotype reversion of myofibroblast-like endothelial cells to endothelium, endothelial-mesenchymal transformation is reduced, and fibrosis progress is inhibited; on the other hand, nuclear translocation of mechanical conduction factors is blocked, and mechanical signal channels related to fibrosis are intervened. The nano preparation can effectively reverse malignant crosstalk of mechanical and biochemical signals in fibrotic lung tissues, and provides an innovative and efficient treatment strategy for pulmonary fibrosis.

The present invention belongs to the field of biomedicine technology, and specifically relates to a circSamd4 and its use in the preparation of a drug for treating myocardial fibrosis. In order to screen and obtain circRNA that plays a key role in the process of myocardial fibrosis, so as to provide a drug for preparing myocardial fibrosis, the present invention provides a circSamd4, a vector for reducing the expression of circSamd4, a host cell containing the vector and its use in the preparation of a drug for treating myocardial fibrosis. The present invention discovered for the first time a circSamd4 that plays a key role in the process of myocardial fibrosis, the nucleotide sequence of which is shown in SEQ ID NO: 1 or SEQ ID NO: 2, and verified that knocking down circSamd4 expression can improve the impaired cardiac contractile function caused by thoracic aortic arch stenosis for 4 weeks, reduce myocardial fibrosis, and inhibit the activation of myocardial fibroblasts. It can be used to prepare a drug for treating myocardial fibrosis, and has important practical significance.

The present invention relates to a multimodal non-invasive in vivo system and related method for the characterization of the tissue microenvironment. The system comprises: a multispectral imaging (MSI) camera for superficial spectral screening; a multispectral optoacoustic tomography (MSOT) module for dynamic vascular and perfusion analysis; a Mueller Matrix Polarimetry (MMP) module for extracellular matrix anisotropy assessment; a Raman spectroscopy module for molecular fingerprinting of fibroblast-associated proteins; an optical coherence tomography (OCT) module for morphological and stratigraphic evaluation; an optional Elastic Scattering Spectroscopy (ESS) module for subcellular scattering biomarkers; and a diachronic analysis module for longitudinal monitoring. Data are integrated by an artificial intelligence processing unit to generate quantitative biomarkers of vascularization, extracellular matrix features, immune activity (Langerhans cells) and fibroblast phenotype, distinguishing physiological myofibroblasts from CAF. The invention enables non-nvasive, biopsy-free evaluation of scars, melanocytic lesions, tumor stroma, wound healing and surgical site monitoring.

The invention provides application of a TP receptor inhibitor in preparation of a medicine for treating cardiac fibrosis, and relates to the technical field of biomedicine. According to the application, the key effect of the TP receptor in heart Gli1 + cells is defined, the TP receptor is determined as an anti-fibrosis specific drug target, and the limitation of insufficient targeting of the existing therapy is broken through. By inhibiting a TP receptor, an AMPK signal channel can be effectively activated, and then ubiquitination degradation of a fibrosis-promoting key factor Gli1 protein is promoted, so that generation and activation of myofibroblasts are inhibited from the source, and the fibrosis process is accurately intervened.

The present invention pertains to combination comprising a CD63-binding molecule and a drug and / or a tracer for use in a method of therapy and / or in a method of in-vivo diagnosis, wherein the drug and / or the tracer is delivered to a myofibroblast.

Disclosed herein is a class of molecules termed remodilins that are effective in treating asthma, pulmonary fibrosis, and associated disorders. The molecules ameliorate asthma and pulmonary fibrosis symptoms by various mechanisms, including inhibiting airway smooth muscle contractile protein accumulation, reducing airway constrictor hyperresponsiveness, inhibiting bronchial fibroblast transformation into myofibroblasts, and / or treating or preventing airway or pulmonary fibrosis.

The invention belongs to the technical field of medicines for treating rheumatoid arthritis complications, and particularly relates to a traditional Chinese medicine composition for rheumatoid arthritis interstitial pulmonary lesion as well as a preparation method and application of the traditional Chinese medicine composition. The traditional Chinese medicine composition comprises ginseng, astragalus membranaceus, prepared rehmannia root, schisandra chinensis, radix asteris, white mulberry root-bark, angelica sinensis, eclipta, radix glehniae, salvia miltiorrhiza, turmeric, exocarpium citri rubrum and liquorice. The traditional Chinese medicine composition has the effects of regulating qi and blood and treating both symptoms and root causes, is suitable for the symptoms of lung arthralgia, deficiency of both qi and yin and stasis of veins and collaterals, can obviously relieve the lung function of patients with rheumatoid arthritis interstitial pulmonary disease, reduces the symptom scores of shortness of breath, dry cough and progressive dyspnea, and improves the curative effect. And the progress of RA-ILD can be effectively inhibited by reducing macrophage apoptosis, activating and proliferating myofibroblasts and inhibiting MMT.