ReviewCells2024
Exploring Extracellular Matrix Crosslinking as a Therapeutic Approach to Fibrosis.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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
31 citing papers in PubMed, 23 citations in OpenAlex.
- Integration of nuclear mechanosensing with integrin-extracellular matrix adhesions.Nucleus (Austin, Tex.) · 2026Review
- Early proteomic and metabolic signatures of liver and eye in OAT-deficient mice.Experimental eye research · 2026Article
- Cooperation, Defection, and Collapse: A Multiscale Game Theory Framework for Emphysema Progression.Cells · 2026Review
- Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease.The FEBS journal · 2026Review
- Exploring mechanisms of scar-free skin wound healing in adult zebrafish in comparison to mouse.PLoS genetics · 2026Article
- Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors.Life science alliance · 2026Article
- PCPE1 and PCPE2: When Sequence Similarity Masks Functional Diversity.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Salvianolic Acid B Inhibited LH2 Expression to Reduce Collagen Synthesis in Pulmonary Fibrosis.Journal of cellular and molecular medicine · 2026Article
- Cellular and molecular regulation of fibrotic postoperative abdominal adhesions.American journal of physiology. Cell physiology · 2026Review
- The extracellular matrix: structure, composition, biological functions, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- Activating the Osteoblastic USP26 Pathway Alleviates Multi-Organ Fibrosis by Decreasing Insulin Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Percolation Forces in Lung Inflammation: Determining the Path to Emphysema or Fibrosis.Biomedicines · 2026Review
- From a stem-cell-centered to a niche-centered view: the core role of collagen networks in hair loss and hair follicle miniaturization.Frontiers in cell and developmental biology · 2026Review
- Mechano-immune interactions in musculoskeletal aging: Mechanisms and translational perspectives.Theranostics · 2026Review
- Mechanistic insights into Strontium-90 superficial radiotherapy in keloids: senescence-associated changes and ECM remodeling across cell-matrix scales.Frontiers in pharmacology · 2026Article
- Nanozymes for extracellular matrix and cell sheet engineering: biomedical potential and complementary enzymatic strategies.Frontiers in molecular biosciences · 2026Review
- Collagen in Fibrotic Diseases.Sub-cellular biochemistry · 2026Review
- Tumor Development in Ulcerative Colitis: Perspectives From Biomechanical Characteristics.Development, growth & differentiation · 2025Review
- Shared and Context-Specific Mechanisms of EMT and Cellular Plasticity in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) provides structural support for tissues and regulatory signals for resident cells. ECM requires a careful balance between protein accumulation and degradation for homeostasis. Disruption of this balance can lead to pathological processes such as fibrosis in organs across the body. Post-translational crosslinking modifications to ECM proteins such as collagens alter ECM structure and function. Dysregulation of crosslinking enzymes as well as changes in crosslinking composition are prevalent in fibrosis. Because of the crucial roles these ECM crosslinking pathways play in disease, the enzymes that govern crosslinking events are being explored as therapeutic targets for fibrosis. Here, we review in depth the molecular mechanisms underlying ECM crosslinking, how ECM crosslinking contributes to fibrosis, and the therapeutic strategies being explored to target ECM crosslinking in fibrosis to restore normal tissue structure and function.
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.