ReviewAmerican journal of physiology. Cell physiology2013
Cellular mechanisms of tissue fibrosis. 3. Novel mechanisms of kidney fibrosis.
Review in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 178 citations in OpenAlex.
- Activated platelets promote endothelial dysfunction and monocyte recruitment in early renal microvascular injury.Journal of inflammation (London, England) · 2026Article
- Shear-wave elastography in renal stiffness in children with hematuria and/or proteinuria.Pediatric research · 2025Article
- Article
- ScRNA-Seq Analysis of Tongue Tissues in Chronic Hyperplastic Candidiasis.Journal of dental research · 2025Article
- Ultrasound viscoelastic imaging in the noninvasive quantitative assessment of chronic kidney disease.Renal failure · 2024Article
- Gucy1α1 specifically marks kidney, heart, lung and liver fibroblasts.Scientific reports · 2024Article
- Standardized evaluation methodology for renal cortical blood perfusion in elderly patients using contrast-enhanced ultrasound: A Chinese expert consensus (2024 edition).Aging medicine (Milton (N.S.W)) · 2024Article
- Pathogenic pathways of renal damage in Fabry nephropathy: interplay between immune cell infiltration, apoptosis and fibrosis.Journal of nephrology · 2024Article
- Single-cell sequencing dissects the transcriptional identity of activated fibroblasts and identifies novel persistent distal tubular injury patterns in kidney fibrosis.Scientific reports · 2024Article
- Pericyte detachment and renal congestion involve interstitial injury and fibrosis in Dahl salt-sensitive rats and humans with heart failure.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Effects of caloric restriction and ketogenic diet on renal fibrosis after ischemia/reperfusion injury.Heliyon · 2023Article
- The value of shear wave elasticity and shear wave dispersion imaging to evaluate the viscoelasticity of renal parenchyma in children with glomerular diseases.BMC nephrology · 2023Article
- The PI3K-Akt-mTOR pathway mediates renal pericyte-myofibroblast transition by enhancing glycolysis through HKII.Journal of translational medicine · 2023Article
- Human umbilical cord mesenchymal stem cell exosome-derived miR-874-3p targeting RIPK1/PGAM5 attenuates kidney tubular epithelial cell damage.Cellular & molecular biology letters · 2023Article
- Dual soluble epoxide hydrolase inhibitor - farnesoid X receptor agonist interventional treatment attenuates renal inflammation and fibrosis.Frontiers in immunology · 2023Article
- Macrophage polarization in tissue fibrosis.PeerJ · 2023Review
- Nephroprotective Effects of Selenium Nanoparticles Against Sodium Arsenite-Induced Damages.International journal of nanomedicine · 2023Article
- miR-122-5p Regulates Renal Fibrosis In Vivo.International journal of molecular sciences · 2022Article
- Suppressing the activity ofTranslational pediatrics · 2022Article
- Mechanosensitive Piezo1 channels mediate renal fibrosis.JCI insight · 2022Article
46 more citing papers are in PubMed but not listed here.
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, defined as loss of kidney function for more than three months, is characterized pathologically by glomerulosclerosis, interstitial fibrosis, tubular atrophy, peritubular capillary rarefaction, and inflammation. Recent studies have identified a previously poorly appreciated, yet extensive population of mesenchymal cells, called either pericytes when attached to peritubular capillaries or resident fibroblasts when embedded in matrix, as the progenitors of scar-forming cells known as myofibroblasts. In response to sustained kidney injury, pericytes detach from the vasculature and differentiate into myofibroblasts, a process not only causing fibrosis, but also directly contributing to capillary rarefaction and inflammation. The interrelationship of these three detrimental processes makes myofibroblasts and their pericyte progenitors an attractive target in chronic kidney disease. In this review, we describe current understanding of the mechanisms of pericyte-to-myofibroblast differentiation during chronic kidney disease, draw parallels with disease processes in the glomerulus, and highlight promising new therapeutic strategies that target pericytes or myofibroblasts. In addition, we describe the critical paracrine roles of epithelial, endothelial, and innate immune cells in the fibrogenic process.
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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.