ReviewExpert review of cardiovascular therapy2016
Myofibroblast secretome and its auto-/paracrine signaling.
Review in Expert review of cardiovascular therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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
23 citing papers in PubMed, 39 citations in OpenAlex.
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- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026Review
- Tcf21 modulates fibroblast activation and promotes cardiac fibrosis after injury via Pdgfrb signaling.Scientific reports · 2025Article
- Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches.Nature reviews. Cardiology · 2025Review
- Lethal Arrhythmogenic Role of Left Ventricular Myocardial Interstitial Fibrosis in Apolipoprotein E/Low-Density Lipoprotein Receptor Double-Knockout Mice with Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2024Article
- CaBiomolecules · 2024Review
- Proteomic Characterization of Corneal Epithelial and Stromal Cell-Derived Extracellular Vesicles.International journal of molecular sciences · 2024Article
- The compound losartan cream inhibits scar formation via TGF-β/Smad pathway.Scientific reports · 2022Article
- Extracellular Vesicles Secreted by Corneal Myofibroblasts Promote Corneal Epithelial Cell Migration.International journal of molecular sciences · 2022Article
- Treatment of myocardial interstitial fibrosis in pathological myocardial hypertrophy.Frontiers in pharmacology · 2022Review
- Cardiac Fibrosis in the Pressure Overloaded Left and Right Ventricle as a Therapeutic Target.Frontiers in cardiovascular medicine · 2022Review
- DYNAMIC BIOREACTOR MODEL TO MIMIC EARLY CARDIAC FIBROSIS IN DIABETES.Journal of mechanics in medicine and biology · 2021Article
- Cardiac fibrosis: Myofibroblast-mediated pathological regulation and drug delivery strategies.Advanced drug delivery reviews · 2021Review
- Exosomal NNMT from peritoneum lavage fluid promotes peritoneal metastasis in gastric cancer.The Kaohsiung journal of medical sciences · 2021Article
- Collagen fibril abnormalities in human and mice abdominal aortic aneurysm.Acta biomaterialia · 2020Article
- Myocardial Interstitial Fibrosis in Nonischemic Heart Disease, Part 3/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020Review
- Cell fibers promote proliferation of co-cultured cells on a dish.Scientific reports · 2020Article
- CaJournal of cardiovascular development and disease · 2019Review
- Xin-Ji-Er-Kang Alleviates Myocardial Infarction-Induced Cardiovascular Remodeling in Rats by Inhibiting Endothelial Dysfunction.BioMed research international · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Myofibroblasts (myoFb) are phenotypically transformed, contractile fibroblast-like cells expressing α-smooth muscle actin microfilaments. They are integral to collagen fibrillogenesis with scar tissue formation at sites of repair irrespective of the etiologic origins of injury or tissue involved. MyoFb can persist long after healing is complete, where their ongoing turnover of collagen accounts for a progressive structural remodeling of an organ (a.k.a. fibrosis, sclerosis or cirrhosis). Such persistent metabolic activity is derived from a secretome consisting of requisite components in the de novo generation of angiotensin (Ang) II. Autocrine and paracrine signaling induced by tissue AngII is expressed via AT1 receptor ligand binding to respectively promote: i) regulation of myoFb collagen synthesis via the fibrogenic cytokine TGF-β1-Smad pathway; and ii) dedifferentiation and protein degradation of atrophic myocytes immobilized and ensnared by fibrillar collagen at sites of scarring. Several cardioprotective strategies in the prevention of fibrosis and involving myofibroblasts are considered. They include: inducing myoFb apoptosis through inactivation of antiapoptotic proteins; AT1 receptor antagonist to interfere with auto-/paracrine myoFb signaling or to induce counterregulatory expression of ACE2; and attacking the AngII-AT1R-TGF-β1-Smad pathway by antibody or the use of triplex-forming oligonucleotides.
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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.