Discovery & Development Services for Cardiovascular Diseases

Given the complex pathophysiology and chronic progression of atherosclerosis, well-characterized animal models that faithfully recapitulate key aspects of human disease pathogenesis have become indispensable tools for investigating disease mechanisms and evaluating novel therapeutic interventions. Recent advances in preclinical model development have yielded increasingly sophisticated systems that more accurately mimic human atherosclerotic progression, enabling rigorous investigation of disease pathogenesis and accelerating the discovery of innovative treatment strategies.

• Genetically Manipulated Models of Atherosclerosis
• High-Fat Diet Induced Models of Atherosclerosis
• LPS-induced Animal Models of Atherosclerosis
• Surgery-induced Animal Models of Atherosclerosis

Well-established animal models of hypertension serve as essential tools for investigating hypertensive disorders and their associated complications, with two primary classifications. Genetic hypertension models, which develop elevated blood pressure without external manipulation, provide valuable systems for studying the fundamental mechanisms of essential hypertension and evaluating novel antihypertensive therapies. Experimentally induced hypertension models, created through pharmacological, dietary, or surgical interventions, offer rapid induction timelines and are particularly suited for investigating secondary hypertension mechanisms triggered by specific environmental or pharmacological factors.

• Essential Hypertension Models
• Drug Induced Hypertension Models
• Environmental Induced Hypertension Models
• Surgical Induced Hypertension Models
• Genetically Engineered Hypertension Models

Thrombosis, characterized by pathological intravascular clot formation, represents a critical mechanism underlying major cardiovascular and cerebrovascular events, including acute myocardial infarction and ischemic stroke, through its dual manifestations as arterial and venous thromboembolism. Given the central role of thrombotic processes in numerous life-threatening conditions, well-validated animal models of thrombosis have become indispensable for elucidating disease mechanisms and advancing the development of novel antithrombotic therapies with improved efficacy and safety profiles.

• Inferior Vena Cava Ligation Induced Thrombosis Models
• Inferior Vena Cava Stenosis Induced Thrombosis Models
• Mechanical Injury Induced Thrombosis Models
• Pro-coagulant Intervention Induced Thrombosis Models
• Ferric Chloride (FeCl3) Induced Thrombosis Models

The myocardial ischemia-reperfusion arrhythmia model serves as a well-established preclinical system for investigating ischemic cardiomyopathy pathophysiology, wherein transient coronary occlusion followed by controlled reperfusion induces characteristic electrophysiological disturbances that mimic clinical manifestations of ischemic heart disease. This model specifically recapitulates the pathophysiological cascade of myocardial injury resulting from temporary blood flow interruption and subsequent restoration, providing critical insights into ischemia-reperfusion injury mechanisms and potential therapeutic interventions.

• Coronary Artery Ligation Induced Myocardial Ischemia-Reperfusion Injury (I/R) Models

Many existing antiarrhythmic agents paradoxically exhibit proarrhythmic potential or induce other cardiovascular complications, highlighting the critical need for developing safer and more effective therapeutic alternatives. The establishment of physiologically relevant arrhythmia models is fundamental to this endeavor, with murine models (mice and rats) serving as the predominant preclinical systems due to their conserved cardiac anatomy and electrophysiological properties that closely mirror human pathophysiology, making them indispensable for investigating arrhythmia mechanisms and evaluating novel pharmacological interventions.

• Drug Induced Arrhythmias Models
• Electrical Stimulation Induced Arrhythmias Models
• Surgery Induced Arrhythmias Models

Heart failure arises from diverse etiologies that ultimately impair myocardial contractility, leading to insufficient cardiac output to meet systemic metabolic demands and subsequent development of characteristic clinical manifestations. To recapitulate this complex pathophysiology, researchers have established multiple preclinical models through distinct induction methods, including pharmacological cardiotoxicity, chronic metabolic stress from high-fat diets, and surgical hemodynamic overload via vascular constriction, each exhibiting unique patterns of cardiac functional deterioration and remodeling that mirror specific clinical heart failure phenotypes.

• Essential Heart Failure Animal Models
• High-Fat Diet Induced Heart Failure Models
• Drug Induced Heart Failure Models
• Surgery Induced Heart Failure Models

Hypertrophic cardiomyopathy represents a maladaptive myocardial response to sustained pathological stimuli, characterized by cardiomyocyte hypertrophy and architectural remodeling. To investigate this complex pathophysiology, researchers have established multiple validated preclinical models that accurately recapitulate disease features, including pressure-overload models induced by surgical aortic constriction, pharmacological models utilizing cardiotropic agents, and genetically engineered models with targeted mutations.

• Pressure Overloading Method Induced Hypertrophic Cardiomyopathy Models
• Volumetric Loading Method Induced Hypertrophic Cardiomyopathy Models
• Myocardial Infarction Method Induced Hypertrophic Cardiomyopathy Models
• Chemicals/Drugs Induced Hypertrophic Cardiomyopathy Models

Heart valve disease pathogenesis involves intricate inflammatory and apoptotic pathways, though the precise molecular mechanisms remain incompletely characterized, necessitating the development of physiologically relevant animal models to elucidate disease progression. An optimal preclinical model of valvular pathology should combine rapid induction kinetics with hallmark features of valve inflammation and fibrosis, while demonstrating quantifiable structural abnormalities through advanced imaging modalities to facilitate comprehensive mechanistic and therapeutic investigations.

• Bacterial-Induced Heart Valve Disease Models
• Diet-Induced Heart Valve Disease Models
• Drug-Induced Heart Valve Disease Models

Cardiovascular infections caused by diverse pathogens including bacteria, viruses, mycoplasma, chlamydia, and rickettsia can manifest as distinct clinical entities such as infective endocarditis, myocarditis, pericarditis, valvulopathies, and systemic vasculitis. Contemporary research utilizes pathogen-specific animal models, with enterovirus-infected models (particularly coxsackievirus B3 and EV71 strains) effectively mimicking the clinical progression of viral myocarditis, enabling mechanistic studies of host-pathogen interactions and therapeutic development.

• Animal Models of Infective Endocarditis
• Animal Models of Infectious Myocarditis
• Animal Models of Systemic Infection