ArticleEuropean journal of histochemistry : EJH2016
Species diversity regarding the presence of proximal tubular progenitor cells of the kidney.
Article in European journal of histochemistry : EJH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.Biology direct · 2026Article
- Histochemistry as a versatile research toolkit in biological research, not only an applied discipline in pathology.European journal of histochemistry : EJH · 2018Article
- Histochemistry today: Detection and location of single molecules.European journal of histochemistry : EJH · 2017Article
- Is there still room for novelty, in histochemical papers?European journal of histochemistry : EJH · 2016Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular source for tubular regeneration following kidney injury is a matter of dispute, with reports suggesting a stem or progenitor cells as the regeneration source while linage tracing studies in mice seemingly favor the classical theory, where regeneration is performed by randomly surviving cells. We, and others have previously described a scattered cell population localized to the tubules of human kidney, which increases in number following injury. Here we have characterized the species distribution of these proximal tubular progenitor cells (PTPCs) in kidney tissue from chimpanzee, pig, rat and mouse using a set of human PTPC markers. We detected PTPCs in chimpanzee and pig kidneys, but not in mouse tissue. Also, subjecting mice to the unilateral urethral obstruction model, caused clear signs of tubular injury, but failed to induce the PTPC phenotype in renal tubules.
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