The circulatory system refers to the tissues and organs in the body that transport blood, including the heart and blood vessels. Circulatory system diseases (CSDs) include myocardial infarction (MI), cardiomyopathy, congenital heart disease (CHD), hypertension, atherosclerosis, etc. Various CSDs can eventually progress to heart failure (HF). A variety of cells can secrete exosomes under normal and pathological conditions, which can specifically fuse with target cell membranes and facilitate intercellular communication. In recent years, studies have found that exosomes play an important role in the development of CSDs, and engineered exosomes can protect their contents from degradation, so that the contents can be delivered to target cells in a functionally active state, thereby achieving targeted therapy of CSDs. In the experimental process of these studies, animal models make the pathophysiological changes in the development of diseases more intuitive and are indispensable in revealing disease pathogenic factors, pathogenesis, target therapy and prognosis, drug development, screening, and efficacy evaluation. In particular, choosing a suitable animal model is an important link in the experimental process. Creative Biolabs has been concerned about the research progress of exosomes in CSDs. We keep up with the development of the industry and market demand, and constantly improve and innovate. After years of accumulated experience, we can provide global customers with a variety of CSD animal models.
Fig.1 Exosome-mediated Ldlr mRNA delivery could robustly restore Ldlr expression and thus reverse the phenotype.1,2
We can provide including but not limited to the following CSD animal models for exosome functional research.
CSD Animal Models | Method | Modeling Mechanism | Applicable Animals | Model Features |
---|---|---|---|---|
MI animal models | Induction of drugs such as pituitary hormone, isoproterenol, doxorubicin, and catecholamines | These drugs can cause coronary artery spasms and prompt MI. | Mouse, rat | The method is simple and feasible, and can better simulate the vasoconstriction process of human MI. |
Coronary artery ligation | Ligation of coronary arteries can lead to narrowing or occlusion, resulting in ischemia and necrosis of the myocardium supplied by the coronary arteries, eventually causing MI. | Mouse, rat | This modeling method is mature and easy to operate, and the obstruction site is clear and easy to judge, which is more consistent with the pathological process of MI. The modeling process can be monitored and evaluated in real-time through electrocardiogram, pathology, serum enzymes, etc. | |
Cardiomyopathy animal models | Doxorubicin induction | Doxorubicin is a chemotherapy drug that can cause cardiotoxicity, leading to progressive cardiomyopathy. | Mouse, rat | This model has the advantages of economy, reliability, and time saving, and high-frequency echocardiography can be used to evaluate whether the model is successfully established. |
Furazolidone induction | Furazolidone may oppose the clearance of catecholamines in the body, leading to excessive excitation, degeneration, and necrosis of cardiomyocytes. | Rat | This model is the closest experimental animal model to human dilated cardiomyopathy in the changes of myocardial energy metabolism, myocardial fiber physiological characteristics, Ca2+ metabolism, and the β-receptor adenylate cyclase system. | |
CHD animal models | Spontaneous hypertension rat model | This model is obtained by multigenerational breeding of inbred rats. | Rat | Without special feed, the rats showed obvious narrowing and bending of peripheral arteries, gradual hypertrophy of the heart, and eventually developed high blood pressure. This model is currently an internationally recognized animal model closest to human essential hypertension. |
Deoxycorticosterone acetate induction with simultaneous unilateral nephrectomy | Deoxycorticosterone acetate can inhibit the occurrence of renin-angiotensin, which mediates the increase of blood pressure. Renal ischemia caused by unilateral nephrectomy can exacerbate systemic arteriolar spasm, resulting in persistent and constant hypertension. | Rat | This model is easy to make and the induced hypertension is stable. Simultaneous unilateral nephrectomy can reduce modeling time. | |
Atherosclerosis animal models | High-cholesterol and high-fat diet | Excess cholesterol and fat can cause hyperlipidemia, damage vascular endothelium, and promote the gradual formation of atherosclerotic plaques in the aorta and coronary arteries. | Mouse, rat, rabbit | This model is easy to operate, has a low mortality rate, and can be observed for a long time. |
Apoe knockout model | The lack of Apoe prevents lipoproteins from recognizing and binding to relevant receptors so that the clearance of these lipoproteins is delayed and hyperlipidemia occurs. Hyperlipidemia induces oxidative modification of lipoproteins and promotes the formation of atherosclerotic lesions. | Mouse | These mice developed marked endothelial damage and lipid accumulation with increasing age. Imposing a high cholesterol and high-fat diet will significantly shorten the modeling time. | |
Ldlr knockout model | The lack of Ldlr leads to the increase of lipoprotein in mouse plasma, induces hyperlipidemia, and promotes the formation of atherosclerotic lesions. | Mouse | ||
HF animal models | Aortic arch coarctation surgery | Narrowing of the aortic arch resulted in increased cardiac afterload (aortic pressure), compensatory myocardial hypertrophy, increased ventricular volume, and cardiac enlargement in rats. | Rat | This model is similar to heart failure caused by high blood pressure or aortic valve stenosis in humans. |
Creative Biolabs aims to focus on human life and health and supports the translation of scientific research results to clinics with experimental animal models. We have a group of professional technicians with strong backgrounds, who can provide the most comprehensive CSDs models for customers to choose from according to their actual needs. If you want to study the key role or therapeutic target of exosomes in CSDs in vivo, please contact us with your ideas. We will provide you with one-stop services including exosome extraction, exosome identification, exosome engineering, exosome labeling, and in vivo and in vitro verification of exosomes with first-class services.
References
Exosomes play pivotal roles in intercellular communication within the circulatory system and are implicated in the pathogenesis of various diseases such as cardiovascular diseases, thrombosis, and vascular inflammation. Our service utilizes exosomes to construct disease models that recapitulate key pathological features, enabling the study of disease mechanisms and therapeutic interventions.
Exosomes can be isolated from various biological fluids such as blood, plasma, serum, and urine, which serve as rich sources of disease-associated biomarkers and mediators. Utilizing exosomes for disease modeling offers several advantages, including physiological relevance, ease of isolation, stability, and the ability to capture disease-specific molecular signatures for accurate modeling.
Our service enables the modeling of a wide spectrum of circulatory system diseases, including atherosclerosis, myocardial infarction, heart failure, stroke, and peripheral artery disease, among others. These models closely mimic human pathophysiology by incorporating disease-relevant exosomes that carry biomolecules indicative of disease status, facilitating the study of disease progression and therapeutic interventions.
Circulatory system disease models are constructed by administering disease-associated exosomes to appropriate in vitro or in vivo model systems, such as cell cultures or animal models. Exosome uptake assays, functional assays, histological analysis, and molecular profiling techniques are employed to assess disease-relevant phenotypic changes, molecular alterations, and therapeutic responses.
Yes, our service offers customizable disease models tailored to address specific research questions, therapeutic targets, or experimental requirements. Researchers can choose disease-relevant exosome sources, model systems, disease endpoints, and outcome measures, allowing for flexible study designs and the exploration of diverse research avenues.