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

Cellular Injury I: Introduction

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...

Cellular Injury IV: Necrosis

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

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...

You might also read

Related Articles

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

Sort by

Same author

The dual role of the microbiome in sepsis: A complex interplay between pathogenicity and protection.

Physics of life reviews·2026

Same author

Unraveling the enigma: Post-translational modifications in psychiatric disorders and their regulatory mechanisms.

Journal of translational internal medicine·2026

Same author

Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.

Biomarker research·2026

Same author

The dual balance of the cytokine network: key messengers of immune activation and triggers of cytokine storm.

Biomarker research·2026

Same author

SIRT3 regulates mitochondrial metabolism through deacetylation of SLC25A6 to impact gastric cancer progression and drug resistance.

Journal of translational medicine·2026

Same author

Epigenetic Regulation in Cardiovascular Diseases: Mechanisms and Therapeutic Targets.

MedComm·2026

Same journal

Mitochondrial dysfunction and cellular senescence drive accelerated gestational aging in spontaneous preterm birth: a narrative review.

Apoptosis : an international journal on programmed cell death·2026

Same journal

Taginostat, a new quinolone-based HDAC6 inhibitor, promotes apoptosis of chronic lymphocytic leukemia cells in vitro and in vivo by activating STAT4.

Apoptosis : an international journal on programmed cell death·2026

Same journal

Correction: Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.

Apoptosis : an international journal on programmed cell death·2026

Same journal

Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.

Apoptosis : an international journal on programmed cell death·2026

Same journal

Microglial tunneling nanotubes: an intercellular transfer facilitating mitochondrial dysfunction and neuroinflammation in experimental cerebral malaria.

Apoptosis : an international journal on programmed cell death·2026

Same journal

Copper dysregulation in cardiometabolic disease: copper deficiency versus cuproptosis.

Apoptosis : an international journal on programmed cell death·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jul 2, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

Interplay between ischemia-reperfusion and metabolic reprogramming.

Lei Duan¹, Hui Ao¹, Lizhou Song²

¹Department of Anesthesiology, Xi'an Aerospace Hospital Affiliated of Northwest University, Xi'an City, Shaanxi Province, China.

Apoptosis : an International Journal on Programmed Cell Death

|July 1, 2026

Summary

This summary is machine-generated.

Ischemia-reperfusion injury (IRI) involves metabolic reprogramming, where cells actively regulate injury initiation, amplification, and resolution. Understanding these metabolic shifts offers new therapeutic strategies and biomarkers for organ protection.

Keywords:

Biomarkers Immunometabolism Ischemia–reperfusion injury Metabolic reprogramming Mitochondrial homeostasis Oxidative stress

More Related Videos

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

Related Experiment Videos

Last Updated: Jul 2, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

Area of Science:

Biochemistry
Pathology
Organ Injury

Background:

Ischemia-reperfusion injury (IRI) is a common pathological process linked to acute organ damage.
IRI involves metabolic changes during ischemia (low oxygen) and reperfusion (blood flow restoration).
Mitochondrial dysfunction, oxidative stress, and inflammation are key features of IRI.

Purpose of the Study:

To summarize the bidirectional interactions between IRI and metabolic reprogramming.
To organize current evidence around key metabolic pathways including glucose, lipid, amino acid, and TCA cycle metabolism.
To highlight metabolic events during different IRI stages and their role in cell death and resolution.

Main Methods:

Review of current scientific evidence on IRI and metabolic reprogramming.
Conceptual organization of metabolic topics: glucose, lipid, amino acid, and TCA cycle metabolism.
Focus on metabolic events during ischemic and reperfusion phases, including cell death pathways.

Main Results:

Metabolic reprogramming is an active regulatory process in IRI, not just a passive response.
Key metabolic events include succinate accumulation, ROS generation, and altered mitochondrial function.
Metabolic changes influence immunometabolism, cell death (apoptosis, ferroptosis, pyroptosis), and post-translational modifications.

Conclusions:

A time-staged, cell death-centered metabolomic framework can identify clinical biomarkers for IRI.
Understanding metabolic reprogramming provides insights into therapeutic intervention windows for IRI.
Metabolic reprogramming actively controls IRI initiation, amplification, and resolution, offering novel therapeutic targets.