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@article{Sanghera:2019:10.1242/dmm.036947,
author = {Sanghera, C and Wong, LM and Panahi, M and Sintou, A and Hasham, M and Sattler, S},
doi = {10.1242/dmm.036947},
journal = {Disease Models & Mechanisms},
title = {Cardiac phenotype in mouse models of systemic autoimmunity},
url = {http://dx.doi.org/10.1242/dmm.036947},
volume = {12},
year = {2019}
}

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TY  - JOUR
AB  - Patients suffering from systemic autoimmune diseases are at significant risk of cardiovascular complications. This can be due to systemically increased levels of inflammation leading to accelerated atherosclerosis, or due to direct damage to the tissues and cells of the heart. Cardiac complications include an increased risk of myocardial infarction, myocarditis and dilated cardiomyopathy, valve disease, endothelial dysfunction, excessive fibrosis, and bona fide autoimmune-mediated tissue damage by autoantibodies or auto-reactive cells. There is, however, still a considerable need to better understand how to diagnose and treat cardiac complications in autoimmune patients. A range of inducible and spontaneous mouse models of systemic autoimmune diseases is available for mechanistic and therapeutic studies. For this Review, we systematically collated information on the cardiac phenotype in the most common inducible, spontaneous and engineered mouse models of systemic lupus erythematosus, rheumatoid arthritis and systemic sclerosis. We also highlight selected lesser-known models of interest to provide researchers with a decision framework to choose the most suitable model for their study of heart involvement in systemic autoimmunity.
AU  - Sanghera,C
AU  - Wong,LM
AU  - Panahi,M
AU  - Sintou,A
AU  - Hasham,M
AU  - Sattler,S
DO  - 10.1242/dmm.036947
PY  - 2019///
SN  - 1754-8403
TI  - Cardiac phenotype in mouse models of systemic autoimmunity
T2  - Disease Models & Mechanisms
UR  - http://dx.doi.org/10.1242/dmm.036947
UR  - https://www.ncbi.nlm.nih.gov/pubmed/30858306
UR  - http://hdl.handle.net/10044/1/69285
VL  - 12
ER  -

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