ReviewFrontiers in genetics2021
Linking Oxidative Stress and DNA Damage to Changes in the Expression of Extracellular Matrix Components.
Review in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 138 citations in OpenAlex.
- Integrated bioinformatics and clinical validation of oxidative stress-associated genes in atrial fibrillation and chronic kidney disease.Experimental and therapeutic medicine · 2026Article
- Trophoblast Extracellular Vesicles Rewire Immunity: A Symptom-Relief Avenue for Recessive Dystrophic Epidermolysis Bullosa.Journal of extracellular vesicles · 2026Article
- MIC13-linked cristae disruption causes metabolic failure and early fibrotic remodelling in mitochondrial liver disease.Cell death & disease · 2026Article
- Silk Fibroin Peptides Promote Extracellular Matrix Homeostasis in Photoaging via Modulation of the ITGB1/FAK-TGF-β/Smad Signaling Axis.Molecules (Basel, Switzerland) · 2026Article
- Dysregulated ITGA3/FAK/YAP axis mediates impaired alveolar type II epithelial cells function in COPD.Journal of advanced research · 2026Article
- Integrative machine learning and CRISPR/Cas9 analysis reveals the role of APOE in lipid metabolism-associated kidney fibrosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Deciphering the Pleiotropic Role ofCells · 2026Article
- Glutathione deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia.Pharmacological reports : PR · 2026Review
- ATM-kinase deficiency triggers early multi-compartment remodeling of the cerebellar microenvironment.Acta neuropathologica communications · 2026Article
- Polyethylene nano- and microplastics trigger metabolic stress responses in human vaginal epithelial cells.Cell death discovery · 2026Article
- Article
- From rosemary and coffee to bioactive nanovesicles: exploring new frontiers in food functional ingredients.NPJ science of food · 2026Article
- Targeting Oxidative Stress in Carcinogenesis: Oleanolic Acid and Its Molecular Pathways.Antioxidants (Basel, Switzerland) · 2026Review
- Nanozymes for extracellular matrix and cell sheet engineering: biomedical potential and complementary enzymatic strategies.Frontiers in molecular biosciences · 2026Review
- Article
- Chlorogenic Acid fromLife (Basel, Switzerland) · 2025Article
- Sympathetic-parasympathetic system deregulation theory of aging.npj aging · 2025Review
- Osteogenesis Imperfecta: A Look into the Cerebellum of the Brtl Murine Model.Molecular neurobiology · 2025Article
- Nanotoxicity of Porous Silica Nanoparticles: Physicochemical Properties and Mechanistic Cellular Endpoints.Nanomaterials (Basel, Switzerland) · 2025Review
- Wounds and the Microbiota: The Healing Interplay Between Host and Microbial Communities.International journal of molecular sciences · 2025Review
21 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells are subjected to endogenous [e.g., reactive oxygen species (ROS), replication stress] and exogenous insults (e.g., UV light, ionizing radiation, and certain chemicals), which can affect the synthesis and/or stability of different macromolecules required for cell and tissue function. Oxidative stress, caused by excess ROS, and DNA damage, triggered in response to different sources, are countered and resolved by specific mechanisms, allowing the normal physiological equilibrium of cells and tissues to be restored. One process that is affected by oxidative stress and DNA damage is extracellular matrix (ECM) remodeling, which is a continuous and highly controlled mechanism that allows tissues to readjust in reaction to different challenges. The crosstalk between oxidative stress/DNA damage and ECM remodeling is not unidirectional. Quite on the contrary, mutations in ECM genes have a strong impact on tissue homeostasis and are characterized by increased oxidative stress and potentially also accumulation of DNA damage. In this review, we will discuss how oxidative stress and DNA damage affect the expression and deposition of ECM molecules and conversely how mutations in genes encoding ECM components trigger accumulation of oxidative stress and DNA damage. Both situations hamper the reestablishment of cell and tissue homeostasis, with negative impacts on tissue and organ function, which can be a driver for severe pathological 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.