ArticleBioMed research international2014
Redox signaling as a therapeutic target to inhibit myofibroblast activation in degenerative fibrotic disease.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Fibroproliferative disorders and diabetes: Understanding the pathophysiologic relationship between Peyronie's disease, Dupuytren disease and diabetes.Endocrinology, diabetes & metabolism · 2021Pooled it
- Enzymatic and non-enzymatic oxidation of fibrillar collagen.Redox report : communications in free radical research · 2026Review
- Probiotics and Extracellular Vesicles as Redox Modulators in Wound Healing: From Microbial Therapeutics to Engineered Nanotherapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Lysionotin attenuates bleomycin-induced pulmonary fibrosis by activating AMPK/Nrf2 pathway.Scientific reports · 2025Article
- Cytokine modulation in pelvic organ prolapse and urinary incontinence: from molecular insights to therapeutic targets.Molecular medicine (Cambridge, Mass.) · 2024Review
- Article
- Early growth response 2, a novel target of pelvic organ prolapse, is highly expressed in anterior vaginal wall tissues with pelvic organ prolapse.Histochemistry and cell biology · 2024Article
- The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.The journal of cardiovascular aging · 2023Article
- Potential molecular targets for intervention in pelvic organ prolapse.Frontiers in medicine · 2023Review
- Dimethyl fumarate ameliorates stress urinary incontinence by reversing ECM remodeling via the Nrf2-TGF-β1/Smad3 pathway in mice.International urogynecology journal · 2022Article
- TGF-β activates NLRP3 inflammasome by an autocrine production of TGF-β in LX-2 human hepatic stellate cells.Molecular and cellular biochemistry · 2022Article
- Physiological ROS controls Upd3-dependent modeling of ECM to support cardiac function inScience advances · 2022Article
- Expression of CD44, Transforming Growth Factor-β, and Matrix Metalloproteinases in Women With Pelvic Organ Prolapse.Frontiers in surgery · 2022Article
- TRPV4 Mechanotransduction in Fibrosis.Cells · 2021Review
- The Nrf2 transcription factor: A multifaceted regulator of the extracellular matrix.Matrix biology plus · 2021Review
- Inflammasome as an Effective Platform for Fibrosis Therapy.Journal of inflammation research · 2021Review
- New insights into the pathogenesis of Peyronie's disease: A narrative review.Chronic diseases and translational medicine · 2020Review
- Cellular senescence: A pathogenic mechanism of pelvic organ prolapse (Review).Molecular medicine reports · 2020Review
- Oxidative Stress: A Possible Trigger for Pelvic Organ Prolapse.Journal of immunology research · 2020Review
- Interplay between BMPs and Reactive Oxygen Species in Cell Signaling and Pathology.Biomolecules · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Degenerative fibrotic diseases encompass numerous systemic and organ-specific disorders. Despite their associated significant morbidity and mortality, there is currently no effective antifibrotic treatment. Fibrosis is characterized by the development and persistence of myofibroblasts, whose unregulated deposition of extracellular matrix components disrupts signaling cascades and normal tissue architecture leading to organ failure and death. The profibrotic cytokine transforming growth factor beta (TGFβ) is considered the foremost inducer of fibrosis, driving myofibroblast differentiation in diverse tissues. This review summarizes recent in vitro and in vivo data demonstrating that TGF β-induced myofibroblast differentiation is driven by a prooxidant shift in redox homeostasis. Elevated NADPH oxidase 4 (NOX4)-derived hydrogen peroxide (H2O2) supported by concomitant decreases in nitric oxide (NO) signaling and reactive oxygen species scavengers are central factors in the molecular pathogenesis of fibrosis in numerous tissues and organs. Moreover, complex interplay between NOX4-derived H2O2 and NO signaling regulates myofibroblast differentiation. Restoring redox homeostasis via antioxidants or NOX4 inactivation as well as by enhancing NO signaling via activation of soluble guanylyl cyclases or inhibition of phosphodiesterases can inhibit and reverse myofibroblast differentiation. Thus, dysregulated redox signaling represents a potential therapeutic target for the treatment of wide variety of different degenerative fibrotic disorders.
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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.