Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Necrosis01:16

Necrosis

6.2K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
6.2K

You might also read

Related Articles

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

Sort by
Same author

Understanding provider behavioral responses to capitation prepayment systems: an integrated mixed-methods approach.

Cost effectiveness and resource allocation : C/E·2026
Same author

Activating bulk S/Se/Te positive electrodes by acidic binder-induced Cu corrosion for wide-temperature Na-Chalcogen batteries.

Nature communications·2026
Same author

A preliminary study on quantitative assessment of apical lesion area.

American journal of translational research·2026
Same author

High-Efficiency P(VDF-HFP)-Based Nanocomposite Dielectrics: Embedding PP Chain Segments to Offset the Efficiency Penalty of Ceramic Fillers.

Langmuir : the ACS journal of surfaces and colloids·2026
Same author

Efficacy of biofeedback therapy for chronic constipation in adults: a systematic review and meta-analysis of randomized controlled trials.

Frontiers in medicine·2026
Same author

Danthron prevents pulmonary fibrosis through improving mitochondrial function by upregulating carboxylesterase 3.

Respiratory research·2026
Same journal

Reassessing the Proposed Creatine-PrP Axis in Endometriosis: Methodological and Mechanistic Considerations.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same journal

IL-7R-Enriched Extracellular Vesicles From the Thymus Drive Colitis via Promoting Neutrophil Extracellular Trap Formation.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same journal

Oral Prebiotic Polysaccharide Hydrogels Sustaining Colon Antibody Release Alleviate Inflammatory Bowel Disease.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same journal

Systematic Phosphorus-Driven Structural and Field Engineering of n-a-Si:H for Flexible n-a-Si:H/Te Near-Infrared Photodetectors.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same journal

Chemically Gradient Ordered Nanodomains Enable Large Tensile Ductility in Gigapascal Lightweight Refractory High-Entropy Alloys.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same journal

Single-Molecule Characterization of Bacterial Factor-Dependent Transcription Activation by Rob.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
See all related articles

Related Experiment Video

Updated: Jan 6, 2026

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

1.8K

NARFL Knockout Triggers Ferroptosis-Driven Vascular Endothelial Dysfunction.

Hui Hu1,2, Jing Luo1, Li Yu1

  • 1Center for Gene Diagnosis and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 30, 2025
PubMed
Summary
This summary is machine-generated.

Nuclear prelamin A recognition factor-like (NARFL) deficiency causes ferroptosis and severe vascular endothelial dysfunction. This discovery reveals a new link between iron-sulfur protein assembly and vascular disease, highlighting NARFL as a potential therapeutic target.

Keywords:
NARFLferroptosisgene polymorphismoxidative damagevascular endothelial dysfunction

More Related Videos

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

11.3K

Related Experiment Videos

Last Updated: Jan 6, 2026

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

1.8K
Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

11.3K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Nuclear prelamin A recognition factor-like (NARFL) is essential for cytosolic iron-sulfur (Fe-S) protein assembly (CIA).
  • The role of NARFL in vascular pathophysiology is largely unknown.
  • Iron-sulfur proteins are critical for numerous cellular processes.

Purpose of the Study:

  • To investigate the role of NARFL in vascular endothelial function and pathophysiology.
  • To elucidate the molecular mechanisms by which NARFL deficiency affects vascular health.
  • To explore the clinical relevance of NARFL in vascular diseases.

Main Methods:

  • Gene knockout studies in zebrafish (narfl) and mice (Ciao3).
  • Analysis of Fe-S protein assembly, cellular iron metabolism, oxidative stress, and lipid peroxidation.
  • Assessment of endothelial cell function and ferroptosis.
  • Investigation of NARFL polymorphisms in human vascular disorders.

Main Results:

  • NARFL deficiency in zebrafish and mice leads to embryonic lethality due to severe vascular defects.
  • NARFL loss impairs Fe-S cluster transfer, causing iron overload, oxidative stress, and ferroptosis in endothelial cells.
  • This mechanism is conserved in human endothelial cells and linked to vascular diseases via NARFL polymorphisms.

Conclusions:

  • NARFL is crucial for maintaining endothelial health by regulating Fe-S protein assembly and preventing ferroptosis.
  • A novel CIA-ferroptosis-vascular axis is identified, with NARFL as a key regulator.
  • NARFL represents a potential therapeutic target for vascular endothelial disorders.