Related Experiment Video

Updated: Mar 2, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
11:30

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

Published on: June 2, 2022

2.6K

Activation of the Nrf2-ARE Signaling Pathway Prevents Hyperphosphatemia-Induced Vascular Calcification by Inducing

Li Yao1, Jian Wang1, Bin-Yao Tian1

  • 1Department of Nephrology, The First Hospital of China Medical University, Shenyang 110001, P.R. China.

Journal of Cellular Biochemistry
|May 18, 2017
PubMed

Insights

The nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) pathway activation may prevent vascular calcification by inducing autophagy in smooth muscle cells. This study shows Nrf2-ARE signaling protects against high phosphorus-induced calcification.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Vascular calcification (VC) is a complex process involving smooth muscle cell differentiation.
  • The nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway plays a role in cellular protection.
  • Autophagy is a cellular degradation process that can influence cell fate.

Purpose of the Study:

  • To investigate the role of the Nrf2-ARE signaling pathway in vascular calcification.
  • To determine if Nrf2-ARE signaling induces autophagy in renal vascular smooth muscle cells (VSMCs).
  • To explore the protective effects of Nrf2-ARE activation against hyperphosphatemia-induced VC.

Main Methods:

  • VSMCs were divided into six groups: control, high phosphorus, si-NC, Nrf2-siRNA, over-expressed Nrf2, and NC.
  • RT-PCR was used to measure mRNA expression of Nrf2-ARE pathway genes.
  • Western blotting detected protein levels of apoptosis and osteogenic markers.
  • Transmission electron microscopy visualized autophagosomes.

Main Results:

  • High phosphorus and Nrf2-siRNA groups showed increased calcium, Runx2, BMP2, Nrf2, HO-1, γ-GCS, NQO-1, and LC3II/LC3I expression compared to controls.
  • Nrf2-siRNA group exhibited higher Runx2 and BMP2 but lower Nrf2, HO-1, γ-GCS, NQO-1, and LC3II/LC3I compared to high phosphorus groups.
  • Over-expression of Nrf2 increased Nrf2, NQO-1, HO-1, γ-GCS, LC3II/LC3I expression, and autophagosome numbers.
  • Nrf2-siRNA group had fewer autophagosomes and lower expression of related proteins.

Conclusions:

  • Activation of the Nrf2-ARE signaling pathway induces autophagy in VSMCs.
  • Nrf2-ARE pathway activation may serve as a protective mechanism against hyperphosphatemia-induced vascular calcification.
  • Targeting the Nrf2-ARE pathway could be a potential therapeutic strategy for VC.
Keywords:
AUTOPHAGYHYPERPHOSPHATEMIA-INDUCED VASCULAR CALCIFICATIONNrf2-ARE SIGNALING PATHWAYVASCULAR SMOOTH MUSCLE CELL

More Related Videos

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

20.5K
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.0K

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
10.2K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
8.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.9K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.8K
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
4.5K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
6.8K