NDLI: Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research

Content Provider	Springer Nature Link
Author	Rai, Vikrant Sharma, Poonam Agrawal, Swati Agrawal, Devendra K.
Copyright Year	2016
Abstract	Heart disease causing cardiac cell death due to ischemia–reperfusion injury is a major cause of morbidity and mortality in the United States. Coronary heart disease and cardiomyopathies are the major cause for congestive heart failure, and thrombosis of the coronary arteries is the most common cause of myocardial infarction. Cardiac injury is followed by post-injury cardiac remodeling or fibrosis. Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium and results in both systolic and diastolic dysfunctions. It has been suggested by both experimental and clinical evidence that fibrotic changes in the heart are reversible. Hence, it is vital to understand the mechanism involved in the initiation, progression, and resolution of cardiac fibrosis to design anti-fibrotic treatment modalities. Animal models are of great importance for cardiovascular research studies. With the developing research field, the choice of selecting an animal model for the proposed research study is crucial for its outcome and translational purpose. Compared to large animal models for cardiac research, the mouse model is preferred by many investigators because of genetic manipulations and easier handling. This critical review is focused to provide insight to young researchers about the various mouse models, advantages and disadvantages, and their use in research pertaining to cardiac fibrosis and hypertrophy.
Starting Page	123
Ending Page	145
Page Count	23
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	424
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2016-10-20
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Ischemic reperfusion injury Myocardial infarction Congestive heart failure Cardiac remodeling Cardiac fibrosis and hypertrophy Mouse models Biochemistry Medical Biochemistry Oncology Cardiology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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