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Re-thinking osteoarthritis pathogenesis: what can we learn (and what do we need to unlearn) from mouse models about the mechanisms involved in disease development.
Arthritis Res Ther
April 2023
Department of Medicine, Faculty of Medical & Health Sciences, University of Auckland, Auckland, New Zealand.
Article Synopsis
- Efforts to create disease-modifying drugs for osteoarthritis have struggled due to the failure of promising candidates in clinical trials, highlighting a need to re-examine the pathology of the disease.
- Significant differences exist in the pathways of osteoarthritis between mouse models (like STR/ort and injury-induced) and humans, emphasizing the complexity and heterogeneity in how the disease manifests.
- Key signaling pathways, such as Wnt and TGF-β, vary between species; for example, TGF-β signaling in mice is primarily through TGF-β3, while in humans it operates through TGF-β1, indicating potential discrepancies in treatment approaches.
Engineering of Human Corneal Endothelial Grafts.
Curr Ophthalmol Rep
September 2015
R&D Department, Tissue Tech, Inc., Ocular Surface Center, and Ocular Surface Research & Education Foundation, 7000 SW 97 Ave #212, Miami, FL 33173, USA, Telephone: (305) 274-1299.
Human corneal endothelial cells (HCEC) play a pivotal role in maintaining corneal transparency. Unlike in other species, HCEC are notorious for their limited proliferative capacity after diseases, injury, aging, and surgery. Persistent HCEC dysfunction leads to sight-threatening bullous keratopathy with either an insufficient cell density or retrocorneal membrane due to endothelial-mesenchymal transition (EMT).
View Article and Find Full Text PDFThe interaction between prorenin, renin and the (pro)renin receptor: time to rethink the role in hypertension.
Curr Opin Nephrol Hypertens
March 2012
Laboratory of Molecular Biochemistry of Hypertension, Institut de Recherches Cliniques de Montreal and Department of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Purpose Of Review: Elevated prorenin levels are seen in diabetics with microvascular disease. The discovery of a receptor capable of binding renin and prorenin [(P)RR] and triggering an intracellular signal in the laboratory setting raised the expectation that prorenin might be directly responsible for these vascular disorders. However, there has been substantial disagreement concerning the signaling properties of renin and prorenin and it has been impossible to inactivate the (P)RR gene in mouse to define its function.
View Article and Find Full Text PDFRethinking WNT signaling.
Trends Genet
April 2004
Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Recent research on the WNT signaling pathway warrants a reassessment of the basic mechanism that transmits signal from the membrane-bound receptor to the nucleus. This article incorporates these findings into a revised model for pathway activation. We propose that the control of Axin stability, rather than the control of ZW3 phosphorylation of the Armadillo protein, is the key step in signaling.
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