自引率: 9.9%
被引量: 6878
通过率: 暂无数据
审稿周期: 2
版面费用: 暂无数据
国人发稿量: 暂无数据
投稿须知/期刊简介:
Regular Papers: Matrix Biology will review for publication studies utilizing most scientific technologies including molecular biology, cell biology, immunochemistry, structural biology, computational biology, theoretical biology, and macromolecular chemistry where the subject is extracellular matrix or is substantially related to matrix and its biological role. The journal will publish articles that are scientifically rigorous, complete within some logical framework, address molecular or cellular mechanisms, and present results that are timely and above average significance. Methods without application to a significant project and data on a new species or system similar to results already in the literature will not be accepted as a regular paper but may be suitable as a Short Note. Short Notes: Matrix Biology will also review for publication brief reports that meet the same standards of quality and field of interest as regular papers but have a narrower scope and more focused interest. Examples are: DNA sequence from a new species of special interest where the sequence from another species is in the literature; a probe, assay or method that is particularly novel and useful; a new mutation that broadens understanding in a genetic disease where other mutations are known; and brief results of more than usual interest that will be followed by a more detailed study. Mini Reviews: The aims of the reviews are to: (a) summarize the general concepts in the field; (b) provide a brief summary of the new information in the field; and (c) define unresolved questions and disagreements about currently available data. The mini-reviews will be aimed at the general reader and employ simple but informative diagrams and drawings. The mini-reviews will be of two different types, single mini-reviews that will summarize some new and important discovery in the field, and cluster mini-reviews on a topic that has been under investigation for some time. To ensure that the mini-reviews reflect a consensus to the scientists in the field, they will be published in one or two issues as a series of articles consisting of (a) an Introductory Review by a Special Editor selected for the series; (b) two or more specialized reviews from two or more additional experts in the field and (c) Letters-to-the-Editor by additional experts in the field who will be invited to comment or volunteer to comment on specific issues raised in the reviews. Announcements: Announcements of national or international meetings may be published in Matrix Biology.
期刊描述简介:
Matrix Biology (established in 1980 as Collagen and Related Research) is a cutting-edge journal that is devoted to publishing the latest results in matrix biology research. We welcome articles that reside at the nexus of understanding the cellular and molecular pathophysiology of the extracellular matrix. Matrix Biology focusses on solving elusive questions, opening new avenues of thought and discovery, and challenging longstanding biological paradigms. Papers considered for review, and ultimately for publication, must contain substantial advances supported by mechanistic and functional insights germane to important physiological or pathological processes. These aspects are crucial and required for publication. Matrix Biology welcomes original research articles, brief reports, commentaries, (mini) reviews, and announcements. Please view our Guide for Authors for more information. Reasons to submit your next article to Matrix Biology: The premier journal in matrix biology; published articles have a universal appeal, value, and utility to the researcher community worldwide. High impact metrics: find our current metrics in the left-hand column. An international board of key researchers in the field. Rigorous, fair and efficient peer review process. Your paper your way: no unnecessary formatting requests. Flexible publication: you can choose to publish open access. Rapid publication: your article available online within a week after acceptance. No page charges and no color charges for online version. Option of co-submitting a data article to Data in Brief.
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Hyaluronan and proteoglycan link protein 1 - a novel signaling molecule for rejuvenating aged skin.
The skin seems to rejuvenate upon exposure to factors within the circulation of young organisms. Intrinsic factors that modulate skin aging are poorly understood. We used heterochronic parabiosis and aptamer-based proteomics to identify serum-derived rejuvenating factors. We discovered a novel extracellular function of hyaluronan and proteoglycan link protein 1 (HAPLN1). Its serum levels decreased with age, disturbing the integrity of the skin extracellular matrix, which is predominantly composed of collagen I and hyaluronan; levels of various markers, which decrease in aged skin, were significantly restored in vivo and in vitro by the administration of recombinant human HAPLN1 (rhHAPLN1). rhHAPLN1 protected transforming growth factor beta receptor 2 on the cell surface from endocytic degradation via mechanisms such as regulation of viscoelasticity, CD44 clustering, and hyaluronan cross-linking. Moreover, rhHAPLN1 regulated the levels of nuclear factor erythroid 2-related factor 2, phosphorylated nuclear factor kappa B, and some cyclin-dependent kinase inhibitors such as p16 and p21. Therefore, rhHAPLN1 may act as a novel biomechanical signaling protein to rejuvenate aged skin.
被引量：- 发表：1970
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Myocardial fibrosis from the perspective of the extracellular matrix: mechanisms to clinical impact.
被引量：- 发表：1970
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Hyperglycemic environments directly compromise intestinal epithelial barrier function in an organoid model and hyaluronan (∼35 kDa) protects via a layilin dependent mechanism.
被引量：- 发表：1970
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Fibronectin isoforms promote postnatal skeletal development.
Fibronectin (FN) is a ubiquitous extracellular matrix glycoprotein essential for the development of various tissues. Mutations in FN cause a unique form of spondylometaphyseal dysplasia, emphasizing its importance in cartilage and bone development. However, the relevance and functional role of FN during skeletal development has remained elusive. To address these aspects, we have generated conditional knockout mouse models targeting the cellular FN isoform in cartilage (cFNKO), the plasma FN isoform in hepatocytes (pFNKO), and both isoforms together in a double knockout (FNdKO). We used these mice to determine the relevance of the two principal FN isoforms in skeletal development from postnatal day one to the adult stage at two months. We identified a distinct topological FN deposition pattern in the mouse limb during different gestational and postnatal skeletal development phases, with prominent levels at the resting and hypertrophic chondrocyte zones and in the trabecular bone. Cartilage-specific cFN emerged as the predominant isoform in the growth plate, whereas circulating pFN remained excluded from the growth plate and confined to the primary and secondary ossification centers. Deleting either isoform independently (cFNKO or pFNKO) yielded only relatively subtle changes in the analyzed skeletal parameters. However, the double knockout of cFN in the growth plate and pFN in the circulation of the FNdKO mice significantly reduced postnatal body weight, body length, and bone length. Micro-CT analysis of the adult bone microarchitecture in FNdKO mice exposed substantial reductions in trabecular bone parameters and bone mineral density. The mice also showed elevated bone marrow adiposity. Analysis of chondrogenesis in FNdKO mice demonstrated changes in the resting, proliferating and hypertrophic growth plate zones, consistent alterations in chondrogenic markers such as collagen type II and X, decreased apoptosis of hypertrophic chondrocytes, and downregulation of bone formation markers. Transforming growth factor-β1 and downstream phospho-AKT levels were significantly lower in the FNdKO than in the control mice, revealing a crucial FN-mediated regulatory pathway in chondrogenesis and bone formation. In conclusion, the data demonstrate that FN is essential for chondrogenesis and bone development. Even though cFN and pFN act in different regions of the bone, both FN isoforms are required for the regulation of chondrogenesis, cartilage maturation, trabecular bone formation, and overall skeletal growth.
被引量：- 发表：1970
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Involvement of lysophosphatidic acid-LPA(1)-YAP signaling in healthy and pathological FAPs migration.
Skeletal muscle fibrosis is defined as the excessive accumulation of extracellular matrix (ECM) components and is a hallmark of muscular dystrophies. Fibro-adipogenic progenitors (FAPs) are the main source of ECM, and thus have been strongly implicated in fibrogenesis. In skeletal muscle fibrotic models, including muscular dystrophies, FAPs undergo dysregulations in terms of proliferation, differentiation, and apoptosis, however few studies have explored the impact of FAPs migration. Here, we studied fibroblast and FAPs migration and identified lysophosphatidic acid (LPA), a signaling lipid central to skeletal muscle fibrogenesis, as a significant migration inductor. We identified LPA receptor 1 (LPA1) mediated signaling as crucial for this effect through a mechanism dependent on the Hippo pathway, another pathway implicated in fibrosis across diverse tissues. This cross-talk favors the activation of the Yes-associated protein 1 (YAP) and Transcriptional coactivator with PDZ-binding motif (TAZ), leading to increased expression of fibrosis-associated genes. This study reveals the role of YAP in LPA-mediated fibrotic responses as inhibition of YAP transcriptional coactivator activity hinders LPA-induced migration in fibroblasts and FAPs. Moreover, we found that FAPs derived from the mdx4cv mice, a murine model of Duchenne muscular dystrophy, display a heightened migratory phenotype due to enhanced LPA signaling compared to wild-type FAPs. Remarkably, we found that the inhibition of LPA1 or YAP transcriptional coactivator activity in mdx4cv FAPs reverts this phenotype. In summary, the identified LPA-LPA1-YAP pathway emerges as a critical driver of skeletal muscle FAPs migration and provides insights into potential novel targets to mitigate fibrosis in muscular dystrophies.
被引量：- 发表：1970
