Sex Differences in Animal Models for Cardiovascular Diseases and the Role of Estrogen

Author(s):  
S. Mahmoodzadeh ◽  
D. Fliegner ◽  
E. Dworatzek
Neuroscience ◽  
2013 ◽  
Vol 239 ◽  
pp. 67-83 ◽  
Author(s):  
Y.C. Wu ◽  
R.A. Hill ◽  
A. Gogos ◽  
M. van den Buuse

Author(s):  
Zhenyu Zhai ◽  
Pengtao Zou ◽  
Fuxiang Liu ◽  
Zirong Xia ◽  
Juxiang Li

Cardiomyocyte death is a fundamental progress in cardiomyopathy. However, the mechanism of triggering the death of myocardial cells remains unclear. Ferroptosis, which is the nonapoptotic, iron-dependent, and peroxidation-driven programmed cell death pathway, that is abundant and readily accessible, was not discovered until recently with a pharmacological approach. New researches have demonstrated the close relationship between ferroptosis and the development of many cardiovascular diseases, and several ferroptosis inhibitors, iron chelators, and small antioxidant molecules can relieve myocardial injury by blocking the ferroptosis pathways. Notably, ferroptosis is gradually being considered as an important cell death mechanism in the animal models with multiple cardiomyopathies. In this review, we will discuss the mechanism of ferroptosis and the important role of ferroptosis in cardiomyopathy with a special emphasis on the value of ferroptosis as a potential novel diagnostic and therapeutic target for patients suffering from cardiomyopathy in the future.


Author(s):  
Bruno Rodrigues ◽  
Daniele Jardim Feriani ◽  
Bruno Bavaresco Gambassi ◽  
Maria Claudia Irigoyen ◽  
Kátia De Angelis ◽  
...  

2020 ◽  
Author(s):  
Sebastiano Sciarretta ◽  
Maurizio Forte ◽  
Francesca Castoldi ◽  
Giacomo Frati ◽  
Francesco Versaci ◽  
...  

Abstract Caloric restriction mimetics (CRMs) are emerging as potential therapeutic agents for the treatment of cardiovascular diseases. CRMs include natural and synthetic compounds able to inhibit protein acetyltransferases, to interfere with acetyl coenzyme A biosynthesis, or to activate (de)acetyltransferase proteins. These modifications mimic the effects of caloric restriction, which is associated with the activation of autophagy. Previous evidence demonstrated the ability of CRMs to ameliorate cardiac function and reduce cardiac hypertrophy and maladaptive remodelling in animal models of ageing, mechanical overload, chronic myocardial ischaemia, and in genetic and metabolic cardiomyopathies. In addition, CRMs were found to reduce acute ischaemia–reperfusion injury. In many cases, these beneficial effects of CRMs appeared to be mediated by autophagy activation. In the present review, we discuss the relevant literature about the role of different CRMs in animal models of cardiac diseases, emphasizing the molecular mechanisms underlying the beneficial effects of these compounds and their potential future clinical application.


2016 ◽  
Author(s):  
M Mannelli ◽  
E Rapizzi ◽  
L Canu ◽  
T Ercolino ◽  
V Giache
Keyword(s):  

2020 ◽  
Vol 18 (1) ◽  
pp. 54-59
Author(s):  
R. A. FAYZULLINA ◽  
◽  
K. A. SAFINA ◽  

Sign in / Sign up

Export Citation Format

Share Document