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Heart Failure II: Pathophysiology01:29

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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GDF11 does not rescue aging-related pathological hypertrophy.

Shavonn C Smith1, Xiaoxiao Zhang1, Xiaoying Zhang1

  • 1From the Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA (S.C.S., Xiaoxiao Zhang, Xiaoying Zhang, P.G., T.S., S Mohsin, X.G., A.S., X.C., S.R.H.); and Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT (M.F., P.G., D.H., M.M., J.K., J.T., S.M.W., A.K., S. MacDonnell).

Circulation Research
|September 19, 2015
PubMed
Summary

This study found no evidence of age-related cardiac hypertrophy in healthy old mice. Restoring Growth Differentiation Factor 11 (GDF11) levels did not improve cardiac structure or function in aged mice.

Keywords:
agingbody weightcardiac function testsgrowth differentiation factorstransforming growth factor beta

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Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Medicine

Background:

  • Growth Differentiation Factor 11 (GDF11) is a secreted factor implicated in aging.
  • Previous research suggested GDF11 levels decline with age and contribute to pathological cardiac hypertrophy (PCH).
  • Restoring GDF11 was proposed to rescue age-related cardiac dysfunction.

Purpose of the Study:

  • To investigate if GDF11 administration can rescue aging-dependent PCH.
  • To elucidate the underlying mechanisms of GDF11's potential effects on cardiac aging.

Main Methods:

  • Old C57BL/6 mice received daily injections of recombinant GDF11 or vehicle for 28 days.
  • Cardiac structure, function, and myocyte size were assessed.
  • In vitro studies examined GDF11's effect on neonatal rat ventricular myocytes exposed to phenylephrine.

Main Results:

  • GDF11 treatment did not alter heart weight, body weight, or heart weight/body weight ratios in old mice.
  • No significant differences were observed in PCH markers, ejection fraction, or ventricular dimensions.
  • In vitro, GDF11 did not reduce but rather induced hypertrophy in neonatal rat ventricular myocytes.

Conclusions:

  • Healthy 24-month-old mice do not exhibit age-related PCH.
  • Restoring GDF11 levels in old mice had no beneficial effect on cardiac structure or function.
  • GDF11 may not be a viable therapeutic target for age-related cardiac hypertrophy.