ArticleJournal of advanced research2023
Single-cell analysis reveals lysyl oxidase (Lox)
Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 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
- Reprogramming the Tumor Oncobiosphere: Bioactive Nanohybrid Materials for Reversing Therapeutic Pseudo-Resistance.ACS omega · 2026Review
- Myeloid Cdc42 deficiency-mediated macrophage pyroptosis exacerbates diabetic cardiomyopathy in type 1 diabetes mellitus.Cardiovascular diabetology · 2026Article
- Xuefu Zhuyu Decoction Reduces Excessive Collagen Deposition and Crosslinking in Myocardial Fibrosis via CTR1-Copper-LOX Axis.Chinese journal of integrative medicine · 2026Article
- Cellular Senescence and the SASP in HFpEF: Pathogenic Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- snRNA-seq identifies Fmo2npj metabolic health and disease · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Fto-mediated m6A demethylation of Lox drives atrial fibrosis and promotes atrial fibrillation in a murine model of hyperthyroidism.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Article
- Transcriptional Heterogeneity of Cardiac Remodeling Between Type 1 and Type 2 Diabetes.Biomedicines · 2026Article
- Connective tissue disorders and cardiac arrhythmias: genetic pathways, mechanistic bridges, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- Remodeling of Cardiac Macrophage Subsets Serves as a Critical Driver of Early Diabetic Myocardial Injury.Journal of inflammation research · 2026Article
- Integrated Bioinformatic and Experimental Identification of DHCR24 and NRG1 as Key Cellular Aging Genes in Diabetic Cardiomyopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Integrated Multi-Omics Analysis Identifies PDK4 and ACOT1 as Metabolic Hub Genes Associated With Myocardial Fibrosis in Diabetic Cardiomyopathy.Journal of diabetes research · 2026Article
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- The interaction between sarcoplasmic reticulum and mitochondria: a novel mechanism for cardiac arrhythmia.Frontiers in physiology · 2026Review
- O-GlcNAcylation in diabetic cardiac remodeling and a proposed endothelial-macrophage-fibroblast network.Frontiers in immunology · 2026Review
- GPR4 promotes immune exclusion in colon cancer through LOXL2-mediated extracellular matrix remodeling.Nature communications · 2025Article
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- Single cell and spatial transcriptomic profiling of the type 2 diabetic coronary microcirculation and myocardium.Basic research in cardiology · 2025Article
- The "dual personality" of LOXL3: a tumor accomplice and a new hope for immunotherapy.Human cell · 2025Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMyocardial fibrosis and cardiac dysfunction are the main characteristics of diabetic heart disease. However, the molecular mechanisms underlying diabetic myocardial fibrosis remain unclear.
objectivesThis study aimed to investigate the heterogeneity of cardiac fibroblasts in diabetic mice and its possible mechanism in the development of diabetic myocardial fibrosis.
methodsWe established a diabetic mouse model by injecting mice with streptozotocin. The overall cell profiles in diabetic hearts were analyzed using single-cell RNA transcriptomic techniques. Cardiac function was evaluated by echocardiography. Cardiac fibrosis was assessed by Masson's trichrome and Sirius red staining. Protein expression was analyzed using Western blotting and immunofluorescence staining.
resultsA total of 11,585 cells were captured in control (Ctrl) and diabetic (DM) hearts. Twelve cell types were identified in this study. The number of fibroblasts was significantly higher in the DM hearts than in the Ctrl group. The fibroblasts were further re-clustered into nine subsets. Interestingly, cluster 4 fibroblasts were significantly increased in diabetic hearts compared with other fibroblast clusters. Lysyl oxidase (Lox) was highly expressed in DM fibroblasts (especially in cluster 4). Beta-aminopropionitrile, a Lox inhibitor, inhibited collagen expression and alleviated cardiac dysfunction in the diabetic group. Lysyl oxidase inhibition also reduced high glucose-induced collagen protein upregulation in primary fibroblasts. Moreover, a TGF-β receptor inhibitor not only prevented an increase in Lox and Col I but also inhibited the phosphorylation of Smad2/3 in fibroblasts.
conclusionsThis study revealed the heterogeneity of cardiac fibroblasts in diabetic mice for the first time. Fibroblasts with high expression of Lox (cluster 4 fibroblasts) were identified to play a crucial role in fibrosis in diabetic heart disease. The findings of this study may provide a possible therapeutic target for interstitial 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.