Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Diabetic Nephropathy

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

Transducer Mechanism: Enzyme-Linked Receptors

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:

Regulation of Angiogenesis and Blood Supply

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 hydroxylase and factor...

You might also read

Related Articles

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

Sort by

Same author

Design and Control of a 1-DOF MRI Compatible Pneumatically Actuated Robot with Long Transmission Lines.

IEEE/ASME transactions on mechatronics : a joint publication of the IEEE Industrial Electronics Society and the ASME Dynamic Systems and Control Division·2011

Same author

Effect of oxidized low-density lipoprotein concentration polarization on human smooth muscle cells' proliferation, cycle, apoptosis and oxidized low-density lipoprotein uptake.

Journal of the Royal Society, Interface·2011

Same author

Acrolein hydrogenation on Pt(211) and Au(211) surfaces: a density functional theory study.

Physical chemistry chemical physics : PCCP·2011

Same author

Anhydrous proton-conducting membrane based on poly-2-vinylpyridinium dihydrogenphosphate for electrochemical applications.

The journal of physical chemistry. B·2011

Same author

Pharmacophore identification, virtual screening and biological evaluation of prenylated flavonoids derivatives as PKB/Akt1 inhibitors.

European journal of medicinal chemistry·2011

Same author

Metabolomic study of insomnia and intervention effects of Suanzaoren decoction using ultra-performance liquid-chromatography/electrospray-ionization synapt high-definition mass spectrometry.

Journal of pharmaceutical and biomedical analysis·2011

Search research articles

Related Experiment Video

Updated: May 28, 2026

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

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

Published on: May 31, 2016

YY1 Promotes Diabetic Vascular Calcification Via m⁶A-Binding Protein HNRNPC.

Bo Yang¹, Xiang Mao², Liqun Ren³

¹Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China; Department of General Internal Medicine, The Affiliated Suzhou Hospital of Nanjing Medical Universily (Suzhou Municipal Hospital, Suzhou Women and Children's Heath Hospital), Suzhou, 215001, China.

Free Radical Biology & Medicine

|May 26, 2026

Summary

Diabetic atherosclerotic calcification is driven by HNRNPC, a key regulator. The transcription factor YY1 promotes this process by increasing HNRNPC expression, highlighting a new therapeutic target for diabetes complications.

Keywords:

Diabetes HNRNPC N6-methyladenosine methylation Vascular calcification YY1

More Related Videos

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

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

Published on: June 2, 2022

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification

Published on: November 20, 2017

Related Experiment Videos

Last Updated: May 28, 2026

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

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

Published on: May 31, 2016

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

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

Published on: June 2, 2022

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification

Published on: November 20, 2017

Area of Science:

Cardiovascular Biology
Molecular Medicine
Endocrinology

Background:

Diabetic atherosclerotic calcification is a fatal complication of diabetes with unclear mechanisms.
Understanding the role of RNA m6A methylation regulatory genes is crucial.

Purpose of the Study:

To investigate the mechanism of HNRNPC in regulating diabetic vascular calcification.
To identify key regulatory factors involved in this process.

Main Methods:

Utilized GEO datasets and mouse transcriptomic data to screen m6A methylation regulatory genes.
Analyzed clinical data correlating serum HNRNPC levels with coronary artery calcium scores.
Employed in vitro and in vivo models to study HNRNPC function in smooth muscle cells and diabetic mice.

Main Results:

HNRNPC was identified as a differentially expressed m6A methylation regulatory gene in both datasets.
Elevated serum HNRNPC levels and coronary artery calcium scores were observed in diabetic patients.
Inhibition of HNRNPC reduced calcification, while its overexpression promoted it. YY1 was found to directly activate HNRNPC transcription, driving calcification.

Conclusions:

HNRNPC plays a critical role in diabetic atherosclerotic calcification.
The transcription factor YY1 promotes vascular calcification by upregulating HNRNPC expression.