Related Experiment Video

Updated: Apr 16, 2026

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

10.9K

Complement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling

Tomokazu Sumida1, Atsuhiko T Naito2, Seitaro Nomura3

  • 11] Department of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan [2] CREST, Japan Science and Technology Agency, Tokyo 102-0075, Japan.

Nature Communications
|February 27, 2015
PubMed

Insights

Complement C1 activates beta-catenin signaling, driving vascular smooth muscle cell proliferation and arterial remodeling in hypertension. Inhibiting this pathway may prevent arteriosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Hypertension causes arterial structural remodeling, leading to arteriosclerosis and end-organ damage.
  • Vascular smooth muscle cell (VSMC) hyperplasia and immune cell infiltration characterize hypertensive arterial remodeling.
  • The exact molecular mechanisms underlying arterial remodeling in hypertension are not fully understood.

Purpose of the Study:

  • To investigate the role of complement C1-induced beta-catenin signaling in hypertensive arterial remodeling.
  • To explore the therapeutic potential of targeting C1-induced beta-catenin signaling.

Main Methods:

  • Utilized genetic (C1qa gene deletion) and chemical inhibition of beta-catenin signaling.
  • Employed macrophage depletion strategies.
  • Monitored blood pressure, VSMC proliferation, and arterial remodeling markers in experimental models.

Main Results:

  • Hypertension induced beta-catenin activation and VSMC proliferation, which were reversed by beta-catenin inhibition.
  • Macrophage depletion and C1qa gene deletion attenuated hypertension-induced beta-catenin signaling, VSMC proliferation, and arterial remodeling.
  • Established a link between complement C1 and arterial remodeling.

Conclusions:

  • Complement C1-induced beta-catenin signaling plays a critical role in hypertensive arterial remodeling.
  • Targeting C1-induced beta-catenin signaling presents a novel therapeutic strategy for preventing arteriosclerosis in hypertensive patients.

More Related Videos

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay11:38

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

3.9K
Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography07:51

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

29.7K

Related Concept Videos

Catenins01:23

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the...
3.3K
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,...
2.3K
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
1.7K
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...
3.1K
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...
1.5K
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
4.8K