スポーツベットアイオー通貨

Support Kyushu U 日本語 ENGLISH Prospective students Current students Companies & researchers Alumni Crisis Management News Events About Office of the President University Overview Kyushu U Connect Fast Facts Public Relations Featured Academics Schools & Centers The Global University Project Alumni Resources Donation Activities and Initiatives Future Plans University Facilities Academics Faculty of Arts and Science Schools Distinctive Education Programs Double Degree Programs Student Exchange Programs Short-term Study Programs The 3 Policies: Diploma, Curriculum, and Admissions Course Registration Academic Calendar Admissions Undergraduate Admissions Graduate Admissions Tuition, Fees & Scholarships Information for International Students Campus Life Facilities and Healthcare Extracurricular / Student-Led Activities Careers & Employment Procedures Contact Information for Consultations Research Research at Kyushu University Academic Staff Educational and Research Activities Database Research Activity Support Industry-University -Government Collaboration Support Research Centers and Projects Framework to Support Collaborated Research Research Integrity 日本語 ENGLISH News Topics Features Research Close-Up Notices Important Research Results Humanities & Social Sciences Art & Design Life & Health Math & Data Physics & Chemistry Materials Technology Environment & Sustainability Events Event Calendar Categories Public Seminar Lecture, etc. Exhibition Other Place Ito Campus Hakozaki Satellite Hospital Campus Chikushi Campus Ohashi Campus Beppu Campus Off Campus About Office of the President Message from the President Kyushu University VISION 2030 Biography Honorary Doctorates History of the Presidency Kyushu U Connect University Overview Organization Charter Presidential Selection Regulations and Policies History Future Plans Mid-Term Objectives and Plans Public Relations Publications Press Releases Promotional Videos University logomark List of Social Media Accounts Virtual Backgrounds Virtual Backgrounds (Archive) Featured Academics Campus Relocation Ceremony to Commemorate Completion of Ito Campus University Facilities Alumni Resources Alumni Associations Donation Donations to Schools, Graduate Schools, and Researchers, etc. Activities and Initiatives Promoting Diversity, Equity, and Inclusion QS-APPLE 2019 Response to the 2016 Kumamoto Earthquake Schools & Centers Research Institutes Centers for Common Education and Research Organizations and Offices Hospitals Libraries Museums Others Academics Faculty of Arts and Science Schools Educational and Research Course The 3 Policies Academic Calendar Course Registration Curriculum Registration / Syllabuses Distinctive Education Programs Program for Leading Graduate Schools Admissions Undergraduate Admissions Enrolling in Undergraduate School Applicants with Disabilities Graduate Admissions Applicants with Disabilities Enrolling as a Research Student Tuition, Fees, & Scholarships Tuition and Fees Enrollment Fee Exemption/Deferment and Tuition Fee Exemption for Newly-enrolled Students Scholarships Payment of tuition Tuition Fee Exemption, Enrollment Fee Exemption/Deferment Financial Aid Double Degree Programs Student Exchange Programs Campus Life Facilities and Healthcare Student Facilities Dormitories Healthcare Personal Accident Insurance for Students/ Liability Insurance Careers & Employment New Information How to use Job and Career Support System Career Consulting Job Hunting Support for International Students Recruitment of International Students Extracurricular / Student-Led Activities Procedures Certificates National Pension System for Students Contact Information for Consultations One-Stop Consultation Service Research Research at Kyushu University Humanities and Social Sciences Art and Design Life and Health Math and Data Physics and Chemistry Materials Technology Environment and Sustainability Research Close-Up Research Centers and Projects Next-Generation Fuel Cell Research Center (NEXT-FC) Research Activity Support On-campus Consultation Research Strategy Promotion Support for Research Funding and Grants Support for Other Research Activities Industry - University - Government Collaboration Support Technological Consultation Intellectual Property Management and Use Joint Research/Sponsored Research Comprehensive Collaboration Joint Research Department Research Integrity Framework to Support Collaborative Research International ･Prospective students ･Current students ･Companies & researchers ･Alumni ･Support Kyushu U Crisis Management ･Contact Us ･Visit ･Career ･Disclaimer & Copyright ･Privacy Policy ･Sitemap 研究成果 Research Results TOP News Research Results The single protein that causes the fibrosis death spiral The single protein that causes the fibrosis death spiral Scientists find VGLL3, a mechanosensitive protein from myofibroblasts, leads to fibrosis in multiple organs 2023.03.22 Research ResultsLife & Health The fibrosis death spiral induced by VGLL3. Myofibroblasts are cells that produce collagen and are key in wound repair. Mechanical stimuli of myofibroblast induces VGLL3 to produce more collagen, resulting in hardening of the extracellular matrix and the tissue. The hardening results in an increase in mechanical stimuli that again induces VGLL3 to produce more collagen. The result is a continuing death spiral of fibrosis. (Nakaya Lab/Kyushu University) Researchers from Kyushu University have found how a single mechanosensitive protein induces the process that thickens and scars tissue, known as fibrosis. The protein, called VGLL3, was shown to contribute to fibrosis in multiple organs. The team hope their findings will lead to new treatments against fibrosis, a pathology that is attributed to 45% of all deaths in industrial nations. Their study was published in Nature Communications. In response to any injury, the body immediately begins a stream of events. Blood coagulates, the tissue begins to inflame, and the body begins to heal. In some cases that healing comes in the form of scaring and hardening. When an injury is on your skin, it shows up as a visible scar, but what happens when vital organs like your heart or liver are damaged and hardens? If left unchecked, it can lead to loss of mechanics and dangerous consequences. These changes in tissues are attributed to the extracellular matrix. The extracellular matrix is a web of proteins found in every cell in the body, and acts both like wires on a circuit that allow cells to communicate with each other, and the beams in a building, giving the organs its structure. Too much extracellular matrix makes the cell, and by extension the organ, tough and inflexible, a condition known as fibrosis. In simple terms, fibrosis is a stiffening of cells and tissue. Its health implications are profound, as it can lead to poor pumping by the heart or cirrhosis in the liver. "Myofibroblasts are a group of cells that produce collagen, a common extracellular matrix protein. In diseased organs they are seen overproducing collagen. Once myofibroblasts appear in diseased organs, fibrosis proceeds in a snowball fashion," says Michio Nakaya Associate Professor at Kyushu University's Faculty of Pharmaceutical Sciences who led the study. "At the same time, myofibroblasts are responsible for proper wound healing." To understand how myofibroblasts turn pathological, Nakaya and his colleagues looked at how different physical stimuli changes the expression of genes in these cells. They found consistent changes in the expression of one gene: VGLL3. Their study showed that after a heart attack, myofibroblasts in both mouse and human hearts express more VGLL3 protein which led to the production of collagen. VGLL3 was also expressed more in fibrotic mouse liver, suggesting it contributes to fibrosis in multiple organs. Conversely, preventing VGLL3 activation in mice led to far less fibrosis in these organs. "We found that VGLL3 is translocated from the cytoplasm to the nucleus and begins to produce collage in response to mechanical stimuli. In mice without VGLL3, the fibrosis after a heart attack was reduced," noted Nakaya. The study further showed that the relationship between matrix stiffness and VGLL3 activation becomes a pathological positive feedback loop, in that a stiffer matrix triggers more VGLL3 activation, which triggers the cell to produce more collagen. Currently, there are only three drugs available for the treatment of fibrosis, and each has its limitations. Considering VGLL3's effects on cell stiffness, Nakaya believes research on treatments should give more attention to this protein. "In the future, we expect to develop drugs and therapies for fibrosis by targeting VGLL3," concludes Nakaya. ### For more information about this research, see "VGLL3 is a mechanosensitive protein that promotes cardiac fibrosis through liquid–liquid phase separation" Yuma Horii, Shoichi Matsuda, Chikashi Toyota, Takumi Morinaga, Takeo Nakaya, Soken Tsuchiya, Masaki Ohmuray, Takanori Hironaka, Ryo Yoshiki, Kotaro Kasai, Yuto Yamauchi, Noburo Takizawa, Akiomi Nagasaka, Akira Tanaka, Hidetaka Kosako, and Michio Nakaya in Nature Communications https://doi.org/10.1038/s41467-023-36189-6 Research-related inquiries Michio Nakaya, Associate ProfessorDepartment of Pharmaceutical Health Care and Sciences, Faculty of Pharmaceutical Sciences Contact information can also be found in the full release. Kyushu U Connect Tweet Back to the list TOP News Research Results The single protein that causes the fibrosis death spiral Research Results Humanities & Social Sciences Art & Design Life & Health Math & Data Physics & Chemistry Materials Technology Environment & Sustainability Year 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 九州大学Kyushu University744 Motooka Nishi-ku Fukuoka 819-0395 Contact Us | Visit Career Academics Disclaimer & Copyright Admissions News Privacy Policy Research Events Sitemap Campus Life About COPYRIGHT © KYUSHU UNIVERSITY. ALL RIGHTS RESERVED.