Related Experiment Video

Updated: Mar 6, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

6.6K

Atorvastatin prevents Angiotensin II induced myocardial hypertrophy in vitro via CCAAT/enhancer-binding protein β

Yintao Chen1, Shasha Yu1, Naijin Zhang1

  • 1Department of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, People's Republic of China.

Biochemical and Biophysical Research Communications
|March 19, 2017
PubMed

Insights

Atorvastatin protects against cardiac hypertrophy by down-regulating CCAAT/enhancer-binding protein β (C/EBPβ). This mechanism rescues mitochondrial function and inhibits apoptosis in cardiomyocytes, offering a new therapeutic target.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Atorvastatin is known to reduce blood lipids and mitigate myocardial hypertrophy and remodeling.
  • CCAAT/enhancer-binding protein β (C/EBPβ) is a key regulator in both physiological and pathological cardiac hypertrophy.

Purpose of the Study:

  • To investigate the role of the C/EBPβ signaling pathway in the cardioprotective effects of atorvastatin on hypertrophic cardiomyocytes.
  • To elucidate the molecular mechanisms underlying atorvastatin's protective action against Angiotensin II-induced cardiac hypertrophy.

Main Methods:

  • Overexpression of C/EBPβ in cardiomyocytes.
  • Assessment of apoptosis rates (early and late).
  • Measurement of mitochondrial membrane potential (MMP).
  • Analysis of Bcl-2/Bax ratio and PGC-1α expression.

Main Results:

  • Overexpression of C/EBPβ abrogated atorvastatin's beneficial effects on Bcl-2/Bax and PGC-1α.
  • In C/EBPβ overexpressing cells, atorvastatin failed to increase Bcl-2/Bax and PGC-1α, leading to increased apoptosis and reduced MMP.
  • Atorvastatin treatment rescued MMP and inhibited apoptosis in Angiotensin II-induced hypertrophic cardiomyocytes.

Conclusions:

  • Atorvastatin exerts a protective effect on hypertrophic cardiomyocytes, potentially through the down-regulation of C/EBPβ.
  • C/EBPβ may serve as a novel therapeutic target for improving mitochondrial function and reducing apoptosis in pathological cardiac hypertrophy.

Keywords:
ApoptosisAtorvastatinC/EBPβMyocardial hypertrophyPGC-1α

More Related Videos

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model10:18

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model

Published on: June 29, 2014

17.7K
Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

39.6K

Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.7K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.9K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.3K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.7K
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
2.0K
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
2.2K