ReviewCell proliferation2021
Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease.
Review in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 43 citations in OpenAlex.
- Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Engineering and Integrating Blood Vessel Organoids: a Comprehensive Blueprint for Physiological and Disease Modeling.Stem cell reviews and reports · 2026Review
- Article
- Exploratory study of dialysis membrane impact on epigenetic methylation patterns in hemodialysis patients using genomic and synchrotron investigations.Scientific reports · 2026Article
- Peripheral Vascular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Thrombospondin 1-CD47 Signalling Modulates Vascular Smooth Muscle Cell Senescence in Chronic Kidney Disease.International journal of molecular sciences · 2026Article
- RhoA accelerates atherosclerosis progression by interacting with Hspa5.Scientific reports · 2026Article
- Bidirectional relationships between increased arterial stiffness and atrial fibrillation.Frontiers in cardiovascular medicine · 2026Article
- The dual role of extracellular vesicles in vascular calcification: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Article
- Bioinspired Collagen/κ-Carrageenan 3D Matrix forACS biomaterials science & engineering · 2025Article
- Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Cellular and molecular mechanisms underlying hemodialysis arteriovenous fistula dysfunction and approaches to promote maturation: a vascular perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Calciprotein particle-activated endothelial cells aggravate smooth muscle cell calcification via paracrine signalling.Cellular and molecular life sciences : CMLS · 2025Article
- The Severity of Carotid Calcifications, but Not Fibroblast Growth Factor 23, Is Associated with Mortality in Hemodialysis: A Single Center Experience.Diseases (Basel, Switzerland) · 2025Article
- Regulation of osteogenic differentiation in vascular smooth muscle cells under high-glucose condition.Frontiers in endocrinology · 2025Review
- Ginsenoside Rb1 attenuates erythropoietin-exacerbated vascular calcification in chronic kidney disease through BMP2-dependent Smad1/5/9 inhibition.CytoJournal · 2025Article
- Understanding Vascular Calcification in Chronic Kidney Disease: Pathogenesis and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Endothelial TGF-β Signaling Regulates Endothelial-Mesenchymal Transition During Arteriovenous Fistula Remodeling in Mice With Chronic Kidney Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Long sleep duration is associated with abdominal aortic calcification among male adults with chronic kidney disease: NHANES 2013-2014.Scientific reports · 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Chronic kidney disease (CKD) is a severe health problem worldwide, and vascular calcification (VC) contributes substantially to the cardiovascular morbidity and high mortality of CKD. CKD is often accompanied by a variety of pathophysiological states, such as inflammation, oxidative stress, hyperglycaemia, hyperparathyroidism and haemodynamic derangement, that can cause injuries to smooth muscle cells (SMCs) and endothelial cells (ECs) to promote VC. Similar to SMCs, whose role has been widely explored in VC, ECs may contribute to VC via osteochondral transdifferentiation, apoptosis, etc. In addition, given their location in the innermost layer of the blood vessel lumen and preferential reception of various pro-calcification stimuli, ECs can pass messages to vascular wall cells and communicate with them. Crosstalk between ECs and SMCs via cytokines through a paracrine mechanism, extracellular vesicles, miRNAs and myoendothelial gap junctions also plays a role in VC. In this review, we emphasize the role of intercellular crosstalk between ECs and SMCs in VC associated with CKD.
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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.