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Angiogenesis requires specific morphogenetic responses of the two principal vascular cell types, namely endothelial cells and mural cells (pericytes and vascular smooth muscle cells), which need to migrate, proliferate, polarize and form a lumen, and deposit a basement membrane.
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The development of an off-the-shelf conduit, without long in vitro culture periods, with proper biological and mechanical properties for coronary bypass surgery is the principal challenge of vascular tissue engineering in current studies.
However, as the principal regulators of vascular permeability, endothelial cells are likely to be involved in systemic increases in permeability.
4, 5 Therefore, accumulation of MRI SVD may be the principal mechanism linking vascular risk factors to cognitive decline.
A more comprehensive mapping of the principal mechanisms underlying vascular formation could reveal new avenues for the engineering of plants with desired body structure and improved biomass production.
Since the glycocalyx is a principal determinant of vascular permeability for macromolecules (e.g. lipoproteins), glycocalyx loss may contribute to the increased transvascular leakage of lipoproteins in patients with type 1 diabetes [ 20].
Introduction: Angiogenesis promotes tumor growth and metastatization and its principal effector is the vascular endothelial growth factor (VEGF) secreted by cancer cells and other components of tumor microenvironment.
We believe all these data suggest that the circulating CD133+CXCR4+CD34- stem cells have a principal role in the vascular homeostasis of the dystrophic skeletal muscle and may partially contribute to muscle regeneration.
VEGF expression driven by hypoxia is considered to be a principal inducer of increased vascular supply to tumours.
The principal proangiogenic factor is vascular endothelial growth factor (VEGF), which can result in increased neovasculature, microvascular permeability, and vasodilatation [ 51– 51].
LMP1 was reported to induce the expression of the principal pro-angiogenic factor vascular endothelial growth factor (VEGF) via the activation of JAK/STAT and MAPK/ERK signaling pathways [38].
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