ArticleThe EMBO journal2015
Loss of MT1-MMP causes cell senescence and nuclear defects which can be reversed by retinoic acid.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.
- The biomedical application of inorganic metal nanoparticles in aging and aging-associated diseases.Journal of advanced research · 2025Pooled it
- Mechanosensing by the nucleus: From pathways to scaling relationships.The Journal of cell biology · 2017Pooled it
- Clearance of p16-positive cardiac cells improves age-related cardiac remodeling in mice.Experimental physiology · 2026Article
- Multi-tissue transcriptomic aging atlas reveals predictive aging biomarkers in the killifish.Nature aging · 2026Article
- Nanoparticle-Based Tools to Study Hallmarks of Aging at the Molecular Level.International journal of nanomedicine · 2026Review
- Impairment of Hyaluronan-Related Glycocalyx Inhibits Macropinocytosis in Cancer Cells via p21 Upregulation.Biomacromolecules · 2025Article
- Functional Analysis of Antipsychotics in Human iPSC-Based Neural Progenitor 2D and 3D Schizophrenia Models.International journal of molecular sciences · 2025Article
- Senescence in the ageing skin: a new focus on mTORC1 and the lysosome.The FEBS journal · 2025Review
- Matrix Metalloproteinases on Skin Photoaging.Journal of cosmetic dermatology · 2024Review
- All-trans retinoic acid inhibits glioblastoma progression and attenuates radiation-induced brain injury.JCI insight · 2024Article
- Mmp14-dependent remodeling of the pericellular-dermal collagen interface governs fibroblast survival.The Journal of cell biology · 2024Article
- Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024Review
- ANTXR1 deficiency promotes fibroblast senescence: implications for GAPO syndrome as a progeroid disorder.Scientific reports · 2024Article
- NatD epigenetically activates FOXA2 expression to promote breast cancer progression by facilitating MMP14 expression.iScience · 2024Article
- Analysis of Membrane Type-1 Matrix Metalloproteinase (MT1-MMP, MMP14) in Eutopic and Ectopic Endometrium and in Serum and Endocervical Mucus of Endometriosis.Biomedicines · 2023Article
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- Computational design of matrix metalloprotenaise-9 (MMP-9) resistant to auto-cleavage.The Biochemical journal · 2023Article
- Extracellular Matrix Dynamics as an Emerging yet Understudied Hallmark of Aging and Longevity.Aging and disease · 2023Review
- Computational design of Matrix Metalloprotenaise-9 (MMP-9) resistant to auto-cleavage.bioRxiv : the preprint server for biology · 2023Article
- Integrin β3-Mediated Cell Senescence Associates with Gut Inflammation and Intestinal Degeneration in Models of Alzheimer's Disease.International journal of molecular sciences · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MT1-MMP (MMP14) is a collagenolytic enzyme located at the cell surface and implicated in extracellular matrix (ECM) remodeling. Mmp14(-/-) mice present dwarfism, bone abnormalities, and premature death. We demonstrate herein that the loss of MT1-MMP also causes cardiac defects and severe metabolic changes, and alters the cytoskeleton and the nuclear lamina structure. Moreover, the absence of MT1-MMP induces a senescent phenotype characterized by up-regulation of p16(INK4a) and p21(CIP1/WAF) (1), increased activity of senescence-associated β-galactosidase, generation of a senescence-associated secretory phenotype, and somatotroph axis alterations. Consistent with the role of retinoic acid signaling in nuclear lamina stabilization, treatment of Mmp14(-/-) mice with all-trans retinoic acid reversed the nuclear lamina alterations, partially rescued the cell senescence phenotypes, ameliorated the pathological defects in bone, skin, and heart, and extended their life span. These results demonstrate that nuclear architecture and cell senescence can be modulated by a membrane protease, in a process involving the ECM as a key regulator of nuclear stiffness under cell stress conditions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.