ReviewBiomolecules2019
Fibroblasts and Their Pathological Functions in the Fibrosis of Aortic Valve Sclerosis and Atherosclerosis.
Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- Biofidelic Simulations of the Ross Procedure: Arterial Growth and Remodeling in an Anatomical Context.International journal for numerical methods in biomedical engineering · 2026Article
- Molecular biology of vascular bioenergetics rewiring: Mitochondrial protective mechanisms of Piper retrofractum in hypertension and oxidative injury.Molecular biology reports · 2026Review
- Complement Component C4B Prioritization Through Drug‒Target Mendelian Randomization and Proteomic Analysis Reveals a Novel Therapeutic Target for Calcific Aortic Valve Stenosis.Cardiovascular drugs and therapy · 2026Article
- Inflammatory Neovascularization and Vascular Remodeling Associated With Carotid Plaque Destabilization.CNS neuroscience & therapeutics · 2026Article
- Zn-Quer Nanozymes Reprogram the Malignant Phenotypic Transformation of Gastric Cancer Cells via Cascade Reactive Oxygen Species Coordination.ACS applied materials & interfaces · 2026Article
- Vascular adventitial cells and vascular remodeling: when a harp of thousand strings does not keep in tune so long.Frontiers in physiology · 2026Review
- Monocytes/Macrophages and Atherogenesis.International journal of molecular sciences · 2025Review
- USP14 Mediates Molecular Mechanisms Regulating Aortic Valve Stenosis Through Ubiquitination.Journal of cellular and molecular medicine · 2025Article
- Incidental Finding of Coronary and Non-Coronary Artery Calcium: What Do Clinicians Need To Know?Current atherosclerosis reports · 2025Review
- Radiation-Induced Cardiac Remodeling: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- Article
- High expression of PLA2G2A in fibroblasts plays a crucial role in the early progression of carotid atherosclerosis.Journal of translational medicine · 2024Article
- Treg Immunomodulation Contributes to the Anti-atherosclerotic Effects of Huxin Formula in ApoEChinese journal of integrative medicine · 2024Article
- Genetic association with autoimmune diseases identifies molecular mechanisms of coronary artery disease.iScience · 2024Article
- Review
- Glutaminolysis regulates endometrial fibrosis in intrauterine adhesion via modulating mitochondrial function.Biological research · 2024Article
- Natural products in atherosclerosis therapy by targeting PPARs: a review focusing on lipid metabolism and inflammation.Frontiers in cardiovascular medicine · 2024Review
- Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization.Frontiers in cardiovascular medicine · 2024Article
- Neutrophil extracellular traps promoting fibroblast activation and aggravating limb ischemia through Wnt5a pathway.American journal of cancer research · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases, such as atherosclerosis and aortic valve sclerosis (AVS) are driven by inflammation induced by a variety of stimuli, including low-density lipoproteins (LDL), reactive oxygen species (ROS), infections, mechanical stress, and chemical insults. Fibrosis is the process of compensating for tissue injury caused by chronic inflammation. Fibrosis is initially beneficial and maintains extracellular homeostasis. However, in the case of AVS and atherosclerosis, persistently active resident fibroblasts, myofibroblasts, and smooth muscle cells (SMCs) perpetually remodel the extracellular matrix under the control of autocrine and paracrine signaling from the immune cells. Myofibroblasts also produce pro-fibrotic factors, such as transforming growth factor-β1 (TGF-β1), angiotensin II (Ang II), and interleukin-1 (IL-1), which allow them to assist in the activation and migration of resident immune cells. Post wound repair, these cells undergo apoptosis or become senescent; however, in the presence of unresolved inflammation and persistence signaling for myofibroblast activation, the tissue homeostasis is disturbed, leading to excessive extracellular matrix (ECM) secretion, disorganized ECM, and thickening of the affected tissue. Accumulating evidence suggests that diverse mechanisms drive fibrosis in cardiovascular pathologies, and it is crucial to understand the impact and contribution of the various mechanisms for the control of fibrosis before the onset of a severe pathological consequence.
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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.