Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

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...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

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,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Resident cardiac stem cells.

Current pharmaceutical design·2011
Same author

Role of stem cells in cardiovascular biology.

Journal of thrombosis and haemostasis : JTH·2011
Same author

The regenerative potential of the human heart.

International journal of cardiology·2004
Same author

Myocyte death and myocyte regeneration in the failing human heart.

Italian heart journal : official journal of the Italian Federation of Cardiology·2001
Same author

Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death.

Diabetes·2001
Same author

Mobilized bone marrow cells repair the infarcted heart, improving function and survival.

Proceedings of the National Academy of Sciences of the United States of America·2001

Related Experiment Video

Updated: Jul 8, 2026

Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
08:42

Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes

Published on: August 28, 2016

Cardiomyocyte aging is gender-dependent: the local IGF-1-IGF-1R system.

A Leri1, J Kajstura, B Li

  • 1Department of Medicine, Vosburgh Pavilion, Room 318, New York Medical College, Valhalla, NY 10595, USA.

Heart Disease (Hagerstown, Md.)
|December 1, 2001
PubMed
Summary

Aging hearts show reduced insulin-like growth factor 1 (IGF-1) and its receptor (IGF-1R) in males, but females maintain higher levels. This difference protects female hearts from age-related damage and dysfunction.

More Related Videos

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
09:41

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes

Published on: February 24, 2017

Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes
09:17

Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes

Published on: October 10, 2020

Related Experiment Videos

Last Updated: Jul 8, 2026

Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
08:42

Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes

Published on: August 28, 2016

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
09:41

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes

Published on: February 24, 2017

Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes
09:17

Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes

Published on: October 10, 2020

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Endocrinology

Background:

  • The insulin-like growth factor 1 (IGF-1) system plays a crucial role in cellular growth and repair.
  • Age-related decline in cardiac function is a significant health concern, with potential sex-specific differences.
  • Understanding the molecular mechanisms underlying cardiac aging is vital for developing targeted interventions.

Purpose of the Study:

  • To investigate the role of the IGF-1 system in the aging process of the heart.
  • To determine if the impact of IGF-1 and its receptor (IGF-1R) on cardiac aging differs between male and female rats.
  • To correlate molecular changes with functional and structural alterations in the aging heart.

Main Methods:

  • Quantification of IGF-1, IGF-1R alpha-subunit, and IGF-1R beta-subunit expression in left ventricular myocytes from male and female Fischer 344 rats across different age groups (3-26 months).
  • Evaluation of myocardial damage, specifically fibrosis, using confocal microscopy in young (3 months) and old (26 months) rats.
  • Assessment of cardiac function through ventricular hemodynamics measurements in a closed-chest preparation.

Main Results:

  • Male myocytes exhibited an 83-84% decrease in IGF-1, IGF-1R alpha, and beta-subunits with aging, while female myocytes showed smaller reductions (28-43%).
  • Aging led to myocardial fibrosis in both sexes, but fibrosis was significantly lower (76-77%) in female hearts compared to male hearts.
  • Senescent male rats displayed cardiac decompensation, whereas old female rats showed only modest ventricular dysfunction.

Conclusions:

  • The enhanced IGF-1-IGF-1R system in female myocytes appears to protect against age-related cardiac damage and dysfunction.
  • Sex-specific differences in the IGF-1 signaling pathway contribute to the divergent aging trajectories of the male and female heart.
  • Preservation of the IGF-1-IGF-1R system may be a key factor in the favorable cardiac aging outcome observed in females.