ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2022
Lysyl oxidase promotes renal fibrosis via accelerating collagen cross-link driving by β-arrestin/ERK/STAT3 pathway.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Bibliometric analysis combined with visualization on universal trends and hot topics of LOX family in human diseases: 1995 to 2025.Frontiers in oncology · 2025Pooled it
- The senescence-stiffening loop: Extracellular matrix remodeling, hypoperfusion, and mitochondrial dysfunction drive tissue aging.Cell metabolism · 2026Review
- Lysyl oxidase (LOX) family proteins in extracellular matrix homeostasis: roles in disease and radiation-induced pathogenesis.Molecular biology reports · 2026Review
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- ATP7A-fibulin-4 complex delivers copper in the Golgi to activate LOX in renal fibrosis.JCI insight · 2026Article
- Is there a link between fascia and cancer? From potential mechanisms to future treatment options.Frontiers in physiology · 2026Review
- Beta-Arrestin 1 Deficiency Enhances Host Anti-Myeloma Immunity Through T Cell Activation and Checkpoint Modulation.International journal of molecular sciences · 2025Article
- Reduced FGF9 Leads to Kidney Injury Through Regulating Renal Tubular Epithelial Cell EMT in Diabetes.Journal of cellular and molecular medicine · 2025Article
- MTHFD2 stabilizes LOX expression through RNA methylation modification to promote sepsis-induced acute kidney injury progression.Human cell · 2025Article
- LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice.Journal of translational medicine · 2025Article
- Epithelial DPP4 promotes Ang II-driven renal fibrosis by targeting ACE2 activity in the renin-angiotensin system.International journal of biological sciences · 2025Article
- Lysyl Oxidase as a Target to Reduce Graft Failure Post Solid Organ Transplantation, a Potential Target for Novel Treatment.Current medicinal chemistry · 2025Review
- Inflammation-driven mechanisms in endometrial cancer: pathways from inflammatory microenvironment remodeling to immune escape.Frontiers in immunology · 2025Review
- Identification of common and specific fibrosis-related genes in three common chronic kidney diseases.Renal failure · 2024Article
- Process-Specific Blood Biomarkers and Outcomes in COVID-19 Versus Non-COVID-19 ARDS (APEL-COVID Study): A Prospective, Observational Cohort Study.Journal of clinical medicine · 2024Article
- Unveiling the role of transgelin as a prognostic and therapeutic target in kidney fibrosis via a proteomic approach.Experimental & molecular medicine · 2024Article
- Article
- Immunosuppressive tumor microenvironment and uterine fibroids: Role in collagen synthesis.Cytokine & growth factor reviews · 2024Review
- Deciphering Collagen Phenotype Dynamics Regulators: Insights from In-Silico Analysis.Journal of bioinformatics and systems biology : Open access · 2024Article
- EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Lysyl oxidase (LOX) is a copper-dependent monoamine oxidase whose primary function is the covalent cross-linking of collagen in the extracellular matrix (ECM). Evidence has shown that LOX is associated with cancer and some fibrotic conditions. We recently found that serum LOX is a potential diagnostic biomarker for renal fibrosis, but the mechanism by which LOX is regulated and contributes to renal fibrosis remains unknown. The current study demonstrates the following: (1) LOX expression was increased in fibrotic kidneys including ischemia-reperfusion injury-(IRI-), unilateral ureteral obstruction-(UUO-), and folic acid- (FA-) induced fibrotic kidneys as well as in the paraffin-embedded sections of human kidneys from the patients with renal fibrosis. (2) The increasing deposition and cross-linking of collagen induced by LOX was observed in IRI-, UUO- and FA-kidneys. (3) LOX was regulated by the β-arrestin-ERK-STAT3 pathway in renal fibrosis. STAT3 was the downstream of AT1R-β-arrestin-ERK, ERK entered the nucleus and activated STAT3-pY705 but not STAT3-pS727. (4) STAT3 nuclear subtranslocation and binding to the LOX promoter may be responsible for the upregulation of LOX expression. (5) Pharmacologic inhibition of LOX with BAPN in vivo inhibited the upregulation of LOX, decreased collagen over cross-linking and ameliorated renal fibrosis after ischemic injury. Collectively, these observations suggest that LOX plays an essential role in the development of renal fibrosis by catalyzing collagen over cross-linking. Thus, strategies targeting LOX could be a new avenue in developing therapeutics against renal fibrosis.
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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.