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

Ischemic Stroke ll: Pathophysiology

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

The Proteasome

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3 (ubiquitin...

The Proteasome

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...

Cerebral Edema ll: Pathophysiology

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

Alzheimer Disease ll: Pathophysiology

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

You might also read

Related Articles

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

Sort by

Same author

Eutrophication mitigation and climate warming coincide with divergent shifts in harmful algal bloom dynamics in Shandong coastal waters.

Water research·2026

Same author

Reprogramming Ion-Transport Dimensionality via Crystal-Channel Engineering to Stabilize Zinc Anodes.

Angewandte Chemie (International ed. in English)·2026

Same author

Functional unblinding in a trial of local tranexamic acid injection during septoplasty.

European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery·2026

Same author

Interpreting survival differences in head and neck squamous cell carcinoma of unknown primary: time-dependent treatment and biological selection.

European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery·2026

Same author

The secretory production of cutinase ICCG-A2 in Corynebacterium glutamicum using acetate as the sole carbon source.

Journal of biotechnology·2026

Same author

Framework Electronegativity Governs Interfacial Transport Kinetics in Lithium-Metal Batteries.

Journal of the American Chemical Society·2026

Search research articles

Related Experiment Video

Updated: May 26, 2026

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Protein degradation pathways after brain ischemia.

Pengfei Ge¹, Fan Zhang, Jingwei Zhao

¹Department of Neurosurgery, First Bethune Hospital of Jilin University, Changchun 130021, China.

Current Drug Targets

|December 30, 2011

Summary

Impaired cellular clearance pathways, including the ubiquitin-proteasomal system (UPS) and autophagy, contribute to organelle failure and neuronal death following brain ischemia. Understanding these mechanisms is crucial for treating ischemic brain injury.

More Related Videos

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

Published on: June 22, 2013

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Published on: May 7, 2015

Related Experiment Videos

Last Updated: May 26, 2026

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

Published on: June 22, 2013

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Published on: May 7, 2015

Area of Science:

Cellular Biology
Neuroscience
Pathology

Background:

Aberrant cellular components are cleared via the ubiquitin-proteasomal system (UPS) or autophagy.
UPS degrades individual proteins; autophagy handles bulk degradation of aggregates and organelles.
Impaired protein degradation is linked to various human diseases.

Purpose of the Study:

To discuss the molecular mechanisms of UPS and autophagy impairment after brain ischemia.
To elucidate how these impairments lead to organelle failure and delayed neuronal death.

Main Methods:

Review of molecular mechanisms underlying protein degradation pathways.
Analysis of the impact of brain ischemia on UPS and autophagy.
Discussion of consequences for cellular integrity and neuronal survival.

Main Results:

Brain ischemia causes protein misfolding, aggregation, and organelle damage.
Ischemia also impairs both the UPS and autophagy pathways.
This dual impairment results in widespread cellular dysfunction.

Conclusions:

Impaired UPS and autophagy are key contributors to organelle failure post-ischemia.
These pathway deficits drive delayed neuronal death.
Targeting protein degradation pathways may offer therapeutic strategies for ischemic stroke.