Matrix metalloproteinase-10: a novel biomarker for idiopathic pulmonary fibrosis

Sokai, Akihiko; Handa, Tomohiro; Tanizawa, Kiminobu; Oga, Toru; Uno, Kazuko; Tsuruyama, Tatsuaki; Kubo, Takeshi; Ikezoe, Kohei; Nakatsuka, Yoshinari; Tanimura, Kazuya; Muro, Shigeo; Hirai, Toyohiro; Nagai, Sonoko; Chin, Kazuo; Mishima, Michiaki

doi:10.1186/s12931-015-0280-9

Cited by 52 publications

(37 citation statements)

References 48 publications

(64 reference statements)

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“…These results are in contrast to prior observations of elevated MMP10 serum levels in patients with idiopathic pulmonary fibrosis (46). However, no symmetry was observed between serum and cellular data, given that MMP10 mRNA and protein expression was driven to a similar extent in EPC-derived ECs among the 3 patients with isolated PAH and the 3 patients with ILDassociated PH.…”

Section: Discussioncontrasting

confidence: 99%

Role of Stromelysin 2 (Matrix Metalloproteinase 10) as a Novel Mediator of Vascular Remodeling Underlying Pulmonary Hypertension Associated With Systemic Sclerosis

Avouac

Guignabert

Hoffmann-Vold

et al. 2017

Arthritis & Rheumatology

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Section: Discussioncontrasting

confidence: 99%

Role of Stromelysin 2 (Matrix Metalloproteinase 10) as a Novel Mediator of Vascular Remodeling Underlying Pulmonary Hypertension Associated With Systemic Sclerosis

Avouac

Guignabert

Hoffmann-Vold

et al. 2017

Arthritis & Rheumatology

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“…These findings suggest that MMP-10 may be a useful biomarker of disease severity and prognosis in patients with idiopathic pulmonary fibrosis. 116 …”

Section: Special Attributes Of Specific Mmpsmentioning

confidence: 99%

Biochemical and Biological Attributes of Matrix Metalloproteinases

Cui

Khalil

2017

Progress in Molecular Biology and Translational Science

943

891

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Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that are involved in the degradation of various proteins in the extracellular matrix (ECM). Typically, MMPs have a propeptide sequence, a catalytic metalloproteinase domain with catalytic zinc, a hinge region or linker peptide, and a hemopexin domain. MMPs are commonly classified on the basis of their substrates and the organization of their structural domains into collagenases, gelatinases, stromelysins, matrilysins, membrane-type (MT)-MMPs, and other MMPs. MMPs are secreted by many cells including fibroblasts, vascular smooth muscle (VSM) and leukocytes. MMPs are regulated at the level of mRNA expression and by activation of their latent zymogen form. MMPs are often secreted as inactive proMMP form which is cleaved to the active form by various proteinases including other MMPs. MMPs cause degradation of ECM proteins such as collagen and elastin, but could influence endothelial cell function as well as VSM cell migration, proliferation, Ca2+ signaling and contraction. MMPs play a role in tissue remodeling during various physiological processes such as angiogenesis, embryogenesis, morphogenesis and wound repair, as well as in pathological conditions such as myocardial infarction, fibrotic disorders, osteoarthritis, and cancer. Increases in specific MMPs could play a role in arterial remodeling, aneurysm formation, venous dilation and lower extremity venous disorders. MMPs also play a major role in leukocyte infiltration and tissue inflammation. MMPs have been detected in cancer, and elevated MMP levels have been associated with tumor progression and invasiveness. MMPs can be regulated by endogenous tissue inhibitors of metalloproteinases (TIMPs), and the MMP/TIMP ratio often determines the extent of ECM protein degradation and tissue remodeling. MMPs have been proposed as biomarkers for numerous pathological conditions and are being examined as potential therapeutic targets in various cardiovascular and musculoskeletal disorders as well as cancer.

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“…Several prognostic/diagnostic biomarkers have been identified in IPF using transcriptional or protein profiling (92)(93)(94)(95)(96). Another emerging technology is measurement of matrix neo-epitopes created during fibrotic remodeling.…”

Section: Novel Peripheral Blood Biomarkersmentioning

confidence: 99%

An Official American Thoracic Society Workshop Report: Use of Animal Models for the Preclinical Assessment of Potential Therapies for Pulmonary Fibrosis

Jenkins

Moore

Chambers

et al. 2017

Am J Respir Cell Mol Biol

299

254

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Numerous compounds have shown efficacy in limiting development of pulmonary fibrosis using animal models, yet few of these compounds have replicated these beneficial effects in clinical trials. Given the challenges associated with performing clinical trials in patients with idiopathic pulmonary fibrosis (IPF), it is imperative that preclinical data packages be robust in their analyses and interpretations to have the best chance of selecting promising drug candidates to advance to clinical trials. The American Thoracic Society has convened a group of experts in lung fibrosis to discuss and formalize recommendations for preclinical assessment of antifibrotic compounds. The panel considered three major themes (choice of animal, practical considerations of fibrosis modeling, and fibrotic endpoints for evaluation). Recognizing the need for practical considerations, we have taken a pragmatic approach. The consensus view is that use of the murine intratracheal bleomycin model in animals of both genders, using hydroxyproline measurements for collagen accumulation along with histologic assessments, is the best-characterized animal model available for preclinical testing. Testing of antifibrotic compounds in this model is recommended to occur after the acute inflammatory phase has subsided (generally after Day 7). Robust analyses may also include confirmatory studies in human IPF specimens and validation of results in a second system using in vivo or in vitro approaches. The panel also strongly encourages the publication of negative results to inform the lung fibrosis community. These recommendations are for preclinical therapeutic evaluation only and are not intended to dissuade development of emerging technologies to better understand IPF pathogenesis.

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Matrix metalloproteinase-10: a novel biomarker for idiopathic pulmonary fibrosis

Cited by 52 publications

References 48 publications

Role of Stromelysin 2 (Matrix Metalloproteinase 10) as a Novel Mediator of Vascular Remodeling Underlying Pulmonary Hypertension Associated With Systemic Sclerosis

Role of Stromelysin 2 (Matrix Metalloproteinase 10) as a Novel Mediator of Vascular Remodeling Underlying Pulmonary Hypertension Associated With Systemic Sclerosis

Biochemical and Biological Attributes of Matrix Metalloproteinases

An Official American Thoracic Society Workshop Report: Use of Animal Models for the Preclinical Assessment of Potential Therapies for Pulmonary Fibrosis

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