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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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...
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...
Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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...
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...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Related Experiment Video

Updated: Jun 4, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
11:53

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Published on: June 14, 2020

Multicellular senescence programs in the aged heart.

Laurent Bultot1, Natsuko Tsurudome1, Emi Kumazaki1

  • 1Department of Cardiovascular Aging, National Cerebral and Cardiovascular Center Research Institute, Osaka, 564-8565, Japan.

Journal of Molecular and Cellular Cardiology Plus
|June 3, 2026
PubMed
Summary
This summary is machine-generated.

Cellular senescence, marked by damage and inflammation, drives cardiac aging and cardiovascular disease. Interventions targeting senescence show promise for restoring heart health.

Keywords:
Cellular senescenceHeartSASPSenolysis

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

Published on: October 10, 2020

Related Experiment Videos

Last Updated: Jun 4, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
11:53

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Published on: June 14, 2020

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
  • Cellular Senescence

Background:

  • Cardiac aging involves molecular damage and stress responses, eroding heart resilience.
  • Genomic instability, telomere dysfunction, and metabolic issues activate immune signaling and cellular senescence.
  • Tissue-level changes include microvascular rarefaction, fibrosis, and hypertrophy, linked to heart conditions like heart failure and atrial fibrillation.

Purpose of the Study:

  • To explore the multifaceted role of cellular senescence in cardiac aging.
  • To understand the context-dependent nature of senescence in the heart.
  • To identify potential therapeutic targets for age-related cardiovascular diseases.

Main Methods:

  • Review of multi-omics and spatial analyses of cardiac senescence.
  • Investigation of non-cell autonomous interactions influencing cardiac aging.
  • Analysis of biomarker discovery, imaging, and epigenetic signatures for cardiac aging.
  • Examination of preclinical intervention studies (senolytics, senomorphics, metabolic).

Main Results:

  • Cardiac senescence is heterogeneous, with both repair-associated and inflammation-propagating phenotypes.
  • Non-cell autonomous interactions significantly modulate cardiac aging trajectories.
  • Biomarkers can quantify cardiac biological aging, though specificity is a challenge.
  • Preclinical interventions demonstrate potential to restore cardiac homeostasis.

Conclusions:

  • Cellular senescence is a key, targetable mechanism in cardiac aging.
  • Understanding senescence heterogeneity is crucial for therapeutic development.
  • Targeting senescence offers a promising avenue for preventing and treating age-related cardiovascular disease.