ReviewCellular reprogramming2013
Cellular transitions and tissue engineering.
Review in Cellular reprogramming, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- The impact of mir200 on extracellular matrix topography-guided epithelial-to-mesenchymal transition of prostate cancer cells.Turkish journal of urology · 2019Article
- Article
- MiR-126a-5p is involved in the hypoxia-induced endothelial-to-mesenchymal transition of neonatal pulmonary hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Lineage tracking of mesenchymal and endothelial progenitors in BMP-induced bone formation.Bone · 2015Article
- Nanoparticle-mediated down-regulation of TWIST increases radiosensitivity of nasopharyngeal carcinoma cells via ERK pathway.American journal of cancer research · 2015Article
- MiR-26a inhibits prostate cancer progression by repression of Wnt5a.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Chitosan hydrogels for chondroitin sulphate controlled release: an analytical characterization.Journal of analytical methods in chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) and endothelial-to-mesenchymal transition (EndMT) describe complex changes in progenitor lineage, cell morphology, and gene expression. Stimulated by environmental cues, these cellular transitions are essential for elements of embryonic development and can be pathologically dysregulated in disease states. EMT occurs in biological processes such as gastrulation, cardiogenesis, and fibrosis. EndMT is involved in development and tissue fibrosis, but recent studies have implicated this process in musculoskeletal biology and pathology. Tissue engineering and regenerative medicine typically rely on endogenous progenitors or progenitors expanded ex vivo to repair damaged or impaired tissues or organs. The processes of EMT and EndMT may aid in elucidating new methods for reducing fibrosis and identifying novel plastic progenitor populations for tissue repair. This review will discuss the potential for EMT and EndMT to impact on tissue engineering and regenerative medicine.
Indexed as
Identifiers
What OpenQuestion holds
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.