ReviewJournal of molecular medicine (Berlin, Germany)2023
The role of immunosuppressive myofibroblasts in the aging process and age-related diseases.
Review in Journal of molecular medicine (Berlin, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Cellular Senescence and Immunosenescence in Melanoma: Insights From the Tumor Microenvironment.Cancer medicine · 2025Pooled it
- The RNA cargo of plasma-derived extracellular vesicles in mCRPC patients captures cancer cells and tumor microenvironment signals.bioRxiv : the preprint server for biology · 2026Article
- Dynamic tRNA modification landscapes reveal METTL1 in fibroblasts as a central regulator of aging.Science China. Life sciences · 2026Article
- New Vistas for Withania somnifera in Signal Transduction of Inflammation and Aging.Pharmaceutical research · 2026Review
- Activating the Osteoblastic USP26 Pathway Alleviates Multi-Organ Fibrosis by Decreasing Insulin Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- B7-H3 (CD276) regulates myeloid-derived suppressor cell differentiation in pulmonary fibrosis.Frontiers in immunology · 2026Article
- Corneal Myofibroblasts Suppress T-Cell Immunity in Corneal Transplantation.Investigative ophthalmology & visual science · 2025Article
- Plasticity and Functional Heterogeneity of Cancer-Associated Fibroblasts.Cancer research · 2025Review
- Inhibition of autotaxin activity with IOA-289 decreases fibrosis in mouse E0771 breast tumors.International journal of cancer · 2025Article
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Diosmetin alleviates osteoarthritis through modulating the polarization of macrophages by inhibiting the PI3K/Akt signaling pathway.Journal of natural medicines · 2025Article
- Reevaluating antiviral thresholds in HBV DNA-negative inactive HBsAg carriers: a multicenter histopathological analysis.Virology journal · 2025Article
- The mechanobiology of fibroblast activation in disease.APL bioengineering · 2025Review
- The emerging role of dysregulated propionate metabolism and methylmalonic acid in metabolic disease, aging, and cancer.Cell metabolism · 2025Review
- Targeting proprotein convertase subtilisin/kexin type 7 in macrophages as a therapeutic strategy to mitigate myocardial infarction-induced inflammation.BMB reports · 2024Article
- Sera from Rheumatoid Arthritis Patients Induce Oxidative Stress and Pro-Angiogenic and Profibrotic Phenotypes in Human Endothelial Cells.Journal of clinical medicine · 2024Article
- Circulating fibrocyte levels correlate with left ventricular mass in middle-aged healthy adults without hypertension.American heart journal plus : cardiology research and practice · 2024Article
- Article
- Single-cell aggrephagy-related patterns facilitate tumor microenvironment intercellular communication, influencing osteosarcoma progression and prognosis.Apoptosis : an international journal on programmed cell death · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue-resident fibroblasts are mesenchymal cells which control the structural integrity of the extracellular matrix (ECM). Fibroblasts possess a remarkable plasticity to allow them to adapt to the changes in the microenvironment and thus maintain tissue homeostasis. Several stresses, also those associated with the aging process, convert quiescent fibroblasts into myofibroblasts which not only display fibrogenic properties but also act as immune regulators cooperating both with tissue-resident immune cells and those immune cells recruited into affected tissues. TGF-β cytokine and reactive oxygen species (ROS) are major inducers of myofibroblast differentiation in pathological conditions either from quiescent fibroblasts or via transdifferentiation from certain other cell types, e.g., macrophages, adipocytes, pericytes, and endothelial cells. Intriguingly, TGF-β and ROS are also important signaling mediators between immunosuppressive cells, such as MDSCs, Tregs, and M2 macrophages. It seems that in pathological states, myofibroblasts are able to interact with the immunosuppressive network. There is clear evidence that a low-grade chronic inflammatory state in aging tissues is counteracted by activation of compensatory immunosuppression. Interestingly, common enhancers of the aging process, such as oxidative stress, loss of DNA integrity, and inflammatory insults, are inducers of myofibroblasts, whereas anti-aging treatments with metformin and rapamycin suppress the differentiation of myofibroblasts and thus prevent age-related tissue fibrosis. I will examine the reciprocal interactions between myofibroblasts and immunosuppressive cells within aging tissues. It seems that the differentiation of myofibroblasts with age-related harmful stresses enhances the activity of the immunosuppressive network which promotes tissue fibrosis and degeneration in elderly individuals.
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.