Circulatory System Disease Model Construction Service for Exosome Functional Research

Overview Services Features FAQs

Overview

The Potential of Exosomes in Circulatory System Disease

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).

Various cells secrete exosomes under normal and pathological conditions, which can specifically fuse with target cell membranes to facilitate intercellular communication. Recent studies have shown that exosomes play a significant role in the development of CSDs, and engineered exosomes can protect their contents from degradation, enabling targeted therapy by delivering active components to target cells. Animal models are essential in these studies for illustrating disease pathophysiology, identifying pathogenic factors, developing targeted therapies, and evaluating drug efficacy. Choosing an appropriate animal model is a crucial step in this 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.

Ldlr mRNA in exosomes reverses the phenotype. (Li, et al., 2021)Fig.1 Exosome-mediated Ldlr mRNA delivery could robustly restore Ldlr expression and thus reverse the phenotype.1,2

Services

Creative Biolabs Circulatory System Disease Model Library for Exosome Functional Research

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.

Features

  • Diversified Circulatory System Disease Models
  • Efficient Exosome Research Platform
  • Customized Research Solutions
  • Comprehensive Experimental Support and Data Analysis

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.

FAQs

Q: How can your exosome research platform benefit my study?

A: Our efficient exosome research platform utilizes advanced isolation, labeling, and functional analysis techniques. We can help you study exosomes within different disease models, enabling you to explore their roles in disease progression and their potential use in targeted therapy and diagnostics.

Q: Can you provide a customized research solution for my project?

A: Yes. During the experimental design process, our technical team will carefully consider and design the experimental plan based on your research objectives, data collection requirements, and project details. From selecting the appropriate animal models to optimizing the experimental plan and conducting exosome research, we ensure that each step is closely aligned with your research goals to guarantee reliable, scientific, and meaningful results.

Q: What kind of support do you provide throughout the research process?

A: We have always been dedicated to providing one-stop services, aiming to save our clients both time and effort. Clients no longer need to consult multiple channels or place orders separately. We offer comprehensive services for exosome functional studies in circulatory system disease models. From experimental design and sample processing to data analysis, every step can be efficiently completed through the collaboration of our professional team.

References

  1. Li, Z.; et al. Exosome-based Ldlr gene therapy for familial hypercholesterolemia in a mouse model. Theranostics. 2021, 11(6):2953-2965.
  2. Distributed under Open Access license CC BY 4.0, without modification.
For Research Use Only. Cannot be used by patients.
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