Introduction

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide, of which heart failure (HF) is among the top causes of cardiovascular mortality, accounting for approximately 80000 deaths annually in the United States alone (Virani et al., 2020).
HF is defined as a complex progressive disease that is secondary to abnormal structure and function of the heart, which causes dysfunction of ventricular systolic and/or diastolic function, thus impairing the blood flow capacity of the heart under normal pressure or the ejection capacity meeting the needs of metabolic organs. The four main triggers of HF include ischemic heart disease, hypertensive heart disease, idiopathic dilated cardiomyopathy, and valvular heart disease (Dokainish et al., 2017). Besides, pathogenesis and pathological processes of HF it also involves comorbidities like obesity, type II diabetes, and chronic kidney disease. Despite such complexity of HF pathological mechanism, it is believed that myocardial remodeling, caused by chronic activation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system (SNS) is the key factor in the occurrence and development of HF (Triposkiadis et al., 2009). Myocardial remodeling can initially partially compensate for cardiac function, but with the aggravation of myocardial remodeling, cardiac function gradually changes from compensatory to decompensated, with obvious symptoms and signs characterized by loss of myocytes, hypertrophy and fibrosis.
Indeed, HF therapies developed in the past decades are based on evidence-based approaches to treat HF risk factors and the implementation of treatment with angiotensin-converting enzyme (ACE) inhibitors, β-blockers, coronary vascularization, implantable cardioverter-defibrillators, and cardiac resynchronization therapies. As indicated by data from Kaiser Permanente, the 1-year cardiovascular hospitalization, mortality, and cardiovascular mortality has been improved from 1998 to 2008 but remained high at 29.6%(Virani et al., 2020), although, current diagnosis and treatment strategies are still ineffective in many patients, and drug treatment is associated with many complications and adverse reactions. Therefore, it is necessary to improve the current symptomatic treatment methods by innovating therapies to ideally target the specific pathological mechanism of HF. The exploration of the pathogenesis of HF and the research of HF therapeutic drugs are very dependent on basic and preclinical studies. In these studies, the research on the transformation process from the test bench to the clinical needs highly relevant experimental models to carry out accurate relationship research. In view of the complex causes of heart failure, current animal models used for HF research covers much of the models commonly used for CVDs research. Therefore, this paper firstly starts with a comprehensive overview of different models in various species currently used in HF research and discuss their general applicability. After that,we summarized the preclinical research review of approved drugs for HF, which would provide theoretical and practical guidance for researchers considering preclinical studies for the treatment of HF.