ReviewFrontiers in cell and developmental biology2024
The role of the cytoskeleton in fibrotic diseases.
Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed.
- ITGBL1-MYH9 interaction in hepatic stellate cells acts as a mechanoregulator controlling liver fibrosis in mice.The Journal of clinical investigation · 2026Article
- Biological profiling of structurally diverse LEGO-LPPOs reveals differences in antibacterial activity, cytocompatibility, and in vivo tolerability.The Journal of antibiotics · 2026Article
- Allicin Attenuates Silica-Induced Pulmonary Fibrosis by Targeting the Serpinb2/NF-κB Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Emergence of fibrotic pericytes and their transcriptional regulation in pulmonary fibrosis.Nature communications · 2026Article
- HDAC8-mediated CAPZB desuccinylation enhances cytoskeleton remodeling to promote idiopathic pulmonary fibrosis.Communications biology · 2026Article
- FAM20A Deficiency Drives Transcriptomic Dysregulation and Functional Impairment in Gingival Fibroblasts.Cell proliferation · 2026Article
- A Novel Core-Shell Hydrogel 3D Model for Studying Macrophage Mechanosensing and Foreign Body Giant Cell Formation.Advanced healthcare materials · 2026Article
- EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage.Biomolecules · 2025Article
- Proteomics-Based Investigation of Sexual Dimorphism in Swim Bladder Texture of Chu's Croaker (Foods (Basel, Switzerland) · 2025Article
- Aging and Intestinal Fibrosis: Mechanisms, Implications, and Therapeutic Strategies.Clinical interventions in aging · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is the process whereby cells at a damaged site are transformed into fibrotic tissue, comprising fibroblasts and an extracellular matrix rich in collagen and fibronectin, following damage to organs or tissues that exceeds their repair capacity. Depending on the affected organs or tissues, fibrosis can be classified into types such as pulmonary fibrosis, hepatic fibrosis, renal fibrosis, and cardiac fibrosis. The primary pathological features of fibrotic diseases include recurrent damage to normal cells and the abnormal activation of fibroblasts, leading to excessive deposition of extracellular matrix and collagen in the intercellular spaces. However, the etiology of certain specific fibrotic diseases remains unclear. Recent research increasingly suggests that the cytoskeleton plays a significant role in fibrotic diseases, with structural changes in the cytoskeleton potentially influencing the progression of organ fibrosis. This review examines cytoskeletal remodeling and its impact on the transformation or activation of normal tissue cells during fibrosis, potentially offering important insights into the etiology and therapeutic strategies for fibrotic diseases.
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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.