ArticleThe American journal of pathology2001
Role of atrophic tubules in development of interstitial fibrosis in microembolism-induced renal failure in rat.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Chronic kidney disease in children: an update.Clinical kidney journal · 2023Review
- Up-regulation of PKR pathway contributes to L-NAME induced hypertension and renal damage.Heliyon · 2020Article
- Role of Renal Hypoxia in the Progression From Acute Kidney Injury to Chronic Kidney Disease.Seminars in nephrology · 2019Review
- Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction.Pediatric nephrology (Berlin, Germany) · 2019Review
- Endothelial colony-forming cells and pro-angiogenic cells: clarifying definitions and their potential role in mitigating acute kidney injury.Acta physiologica (Oxford, England) · 2018Review
- Evolutionary Nephrology.Kidney international reports · 2017Article
- Progression of chronic kidney disease: too much cellular talk causes damage.Kidney international · 2017Review
- Mitochondrial Pathology and Glycolytic Shift during Proximal Tubule Atrophy after Ischemic AKI.Journal of the American Society of Nephrology : JASN · 2016Article
- The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.American journal of physiology. Renal physiology · 2016Review
- Tubular atrophy in the pathogenesis of chronic kidney disease progression.Pediatric nephrology (Berlin, Germany) · 2016Review
- Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression.Journal of the American Society of Nephrology : JASN · 2015Review
- Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.Nature reviews. Nephrology · 2015Review
- Increased expression of p21WAF1/CIP1 in kidney proximal tubules mediates fibrosis.American journal of physiology. Renal physiology · 2015Article
- Autophagy regulates TGF-β expression and suppresses kidney fibrosis induced by unilateral ureteral obstruction.Journal of the American Society of Nephrology : JASN · 2014Article
- Severe renal mass reduction impairs recovery and promotes fibrosis after AKI.Journal of the American Society of Nephrology : JASN · 2014Article
- Autophagy in acute kidney injury and repair.Nephron. Clinical practice · 2014Review
- Chronic kidney disease following acute kidney injury-risk and outcomes.Nature reviews. Nephrology · 2013Review
- Targeted proximal tubule injury triggers interstitial fibrosis and glomerulosclerosis.Kidney international · 2012Article
- PTEN loss defines a TGF-β-induced tubule phenotype of failed differentiation and JNK signaling during renal fibrosis.American journal of physiology. Renal physiology · 2012Article
- Myofibroblast differentiation during fibrosis: role of NAD(P)H oxidases.Kidney international · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We explored the origin and participation of atrophic tubules in the progression of interstitial fibrosis using a new microembolic rat model of chronic renal failure in which foci of atrophic tubules with cuff-like basement membrane thickening developed at 4 weeks. Atrophic tubules, immunoreactive for vimentin and platelet-derived growth factor, were surrounded by transformed interstitial cells expressing platelet-derived growth factor receptor beta and alpha-smooth muscle actin. Some tubules in the deep cortex and the outer stripe of the outer medulla had a mosaic appearance. Tall, intact proximal tubular cells with a brush border and positivity for Phaseolus vulgaris erythroagglutinin, adjoined typical atrophic tubule cells having no brush border and an immunostaining pattern characteristic for atrophic tubules. The transformed interstitial cells expressing alpha-smooth muscle actin were located near atrophic but not intact tubular epithelial cells. Type IV collagen accumulated between damaged tubular cells and transformed interstitial cells. Heat shock protein 47 showed immunoreactivity in damaged epithelial cells and in interstitial myofibroblasts. Staining with an anti-endothelial antibody suggested damage to peritubular capillaries near atrophic tubules. By disturbance of microcirculation following microsphere injection, proximal tubular cells expressed vimentin and platelet-derived growth factor; diffusion of the latter presumably stimulated transformation of interstitial cells to myofibroblasts. Injured tubular epithelial cells and interstitial myofibroblasts both were responsible for interstitial fibrosis.
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