Custom Animal Models of Hypertrophic Cardiomyopathy
Basic Research
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* Please note that all of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

Custom Animal Models of Hypertrophic Cardiomyopathy

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In recent years, as the research of hypertrophic cardiomyopathy continues to deepen, more and more animal models of the disease have been applied to the research practice. Ace Therapeutics always pays attention to all kinds of research advances in the field of cardiovascular disease, and is committed to providing diversified development services of animal models of hypertrophic cardiomyopathy to help customers promote basic research and drug discovery of hypertrophic cardiomyopathy.


Overview of Animal Models of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy is an adaptive response of cardiomyocytes to the stimulation of various pathological factors. In its early stages, cardiac hypertrophy is considered a compensatory process for ventricular wall thickening and improved myocardial contractile function. However, under sustained pathological stress, cardiac hypertrophy eventually leads to decompensated heart failure, which poses a serious health risk. At present, researchers have successfully established various models of hypertrophic cardiomyopathy induced by different modeling approaches. For example, surgical narrowing of the aorta is an ideal model to study hypertrophic cardiomyopathy. In addition, chemical/drug-induced animal models and transgenic animal models hold great promise for the study of hypertrophic cardiomyopathy.

Mitochondrial alterations in hypertrophic cardiomyopathyFig. 1 Mitochondrial alterations in hypertrophic cardiomyopathy. (Ranjbarvaziri S, et al., 2021)

Our Services

Ace Therapeutics offers our client with the following development methods for animal models of hypertrophic cardiomyopathy, including but not limited to:

Pressure Overloading Volumetric Loading Myocardial Infarction Chemical/Drugs

Hypertrophic Cardiomyopathy Models Induced by Pressure Overloading Method

  • Overview
    We can choose to perform aortic narrowing surgery on the ascending aorta, aortic arch or abdominal aorta of rats, which leads to elevated blood pressure, increased cardiac afterload, increased oxygen consumption for cardiac functioning, and ultimately triggers myocardial metabolism disorders and left ventricular remodeling to produce myocardial hypertrophy. This method has the advantages of short modeling time, convenient operation and good reproducibility, and it is one of the more commonly used methods for constructing animal models of myocardial hypertrophy.
  • Available Animal Species and Strains
    Rats (SD rats, Wistar rats)
  • Animal Model Validation
    4 to 6 weeks after surgical modeling, the thickness of the ventricular wall in rats was detected by echocardiography, and a significant increase in diastolic ventricular wall thickness, if present, indicated successful modeling.

Hypertrophic Cardiomyopathy Models Induced by Volumetric Loading Method

  • Overview
    We can cause arteriovenous short circuits in experimental animals by surgery, resulting in increased return blood flow, increased cardiac preload, and prolonged stimulation leading to hemodynamic overload causing right ventricular hypertrophy.
  • Available Animal Species and Strains
    Rats (SD rats, Wistar rats)
  • Animal Model Validation
    4 to 6 weeks after completion of the arteriovenous fistula method, we will detect the thickness of the ventricular wall in rats by echocardiography, and if there is a significant increase in the diastolic ventricular wall thickness, it will indicate successful modeling.

Hypertrophic Cardiomyopathy Models Induced by Myocardial Infarction Method

  • Overview
    We are able to artificially block coronary blood flow by ligating the coronary arteries of experimental animals, occluding coronary arteries, or promoting coronary artery thrombosis, resulting in myocardial ischemia and necrosis in the corresponding blood-supplying areas, whereas in the non-ischemic areas compensatory hypertrophy of the myocardium occurs.
  • Available Animal Species and Strains
    Rats (SD rats, Wistar rats)
  • Animal Model Validation
    1 to 2 weeks after the coronary ligation procedure, we will examine the thickness of the ventricular wall in rats by echocardiography, and a significant increase in diastolic ventricular wall thickness will indicate successful modeling.

Hypertrophic Cardiomyopathy Models Induced by Chemicals/Drugs

  • Overview
    We can give specific chemicals or drugs (e.g., norepinephrine, isoprenaline) to experimental animals by injection administration or continuous administration to promote signaling pathways, stimulate the synthesis of regulatory proteins in cardiomyocytes, promote collagen deposition and myocardial fibrosis, and ultimately lead to myocardial hypertrophy in the animal model.
  • Available Animal Species and Strains
    Mice (C57BL/6 mice, BALB/c mice), rats (SD rats, Wistar rats)
  • Animal Model Validation
    Usually, after 2 to 4 weeks of modeling with chemicals or drugs, we can detect the thickness of the ventricular wall in animal models by echocardiography, and if there is a significant increase in the thickness of the ventricular wall in diastole, it indicates that the modeling has been successful.

Ace Therapeutics has extensive experience in building animal models of cardiovascular disease, and we can build animal models of hypertrophic cardiomyopathy according to our clients' customized needs. In addition, our animal models can be used for pharmacokinetic, pharmacodynamic, and toxicological studies of hypertrophic cardiomyopathy. If you are interested in our services, please don't hesitate to contact us.

Reference
  1. Ranjbarvaziri, S.; et al. Altered cardiac energetics and mitochondrial dysfunction in hypertrophic cardiomyopathy. Circulation. 2021, 144(21):1714-1731.
! All of our services and products are intended for preclinical research use only and cannot be intended for any clinical use.
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