Targetable cellular signaling events mediate vascular pathology in vascular Ehlers-Danlos syndrome

Journal
Journal of Clinical Investigation
ISSN
0021-9738
Date Issued
2020
Author(s)
David Goltzman
Type
Resource Types::text::journal::journal article
Scopus ID
2-s2.0-85078868498
WoS ID
WOS:000512418100021
DOI
URL
URL Institutional Repository
Cite this document
Bowen, C. J., Calderón Giadrosic, J. F., Burger, Z., Rykiel, G., Davis, E. C., Helmers, M. R., Benke, K., Gallo MacFarlane, E., & Dietz, H. C. (2019). Targetable cellular signaling events mediate vascular pathology in vascular Ehlers-Danlos syndrome. Journal of Clinical Investigation, 130(2), 686-698. https://doi.org/10.1172/JCI130730
Project(s)
Subjects
animals

; 

aortic rupture

; 

collagen type iii

; 

disease models, animal

; 

ehlers-danlos syndrome

; 

enzyme inhibitors

; 

humans

; 

map kinase signaling system

; 

mice

; 

mice, transgenic

; 

mitogen-activated protein kinase 1

; 

mitogen-activated protein kinase 3

; 

mutation

; 

protein kinase c beta

; 

androgen

; 

glycine

; 

inositol 1,4,5 trisphosphate

; 

mitogen activated protein kinase

; 

mitogen activated protein kinase 1

; 

mitogen activated protein kinase 3

; 

oxytocin

; 

phospholipase c

; 

protein kinase c

; 

protein kinase c beta

; 

transcriptome

; 

col3a1 protein, mouse

; 

collagen type 3

; 

enzyme inhibitor

; 

mapk1 protein, mouse

; 

mapk3 protein, mouse

; 

mitogen activated protein kinase 1

; 

mitogen activated protein kinase 3

; 

prkcb protein, mouse

; 

protein kinase c beta

; 

animal experiment

; 

animal model

; 

aortic rupture

; 

article

; 

cardiovascular risk

; 

controlled study

; 

ehlers danlos syndrome

; 

female

; 

mouse

; 

nonhuman

; 

pregnancy

; 

priority journal

; 

puberty

; 

signal transduction

; 

thoracic aorta

; 

transcriptomics

; 

vascular disease

; 

animal

; 

aortic rupture

; 

disease model

; 

drug effect

; 

ehlers danlos syndrome

; 

genetics

; 

human

; 

mapk signaling

; 

metabolism

; 

mutation

; 

pathology

; 

transgenic mouse