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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

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Stab-Wound Mouse Model for Studying Hemorrhage and Inflammation in Traumatic Brain Injury
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Inflammation Impairs Poststroke Recovery by Disrupting Iron Homeostasis in Brain.

Xin Guo1,2,3,4, Xiaofang Jin1, Shaomeng Kang1

  • 1Laboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Sciences, Hebei Normal University, Shijiazhuang, China.

Antioxidants & Redox Signaling
|June 29, 2026
PubMed
Summary

Inflammation-associated iron dyshomeostasis, particularly Ferroportin 1 (FPN1) deficiency, impairs brain recovery after stroke. This leads to increased neuronal damage and delayed sensorimotor function, highlighting iron metabolism

Keywords:
blood–brain barrierendogenous repair mechanismferroportin 1inflammationstroke

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Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:22

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Microglial activation initiates inflammatory responses often linked to iron metabolism imbalance.
  • Iron dyshomeostasis is a potential contributor to poor outcomes following stroke.

Purpose of the Study:

  • To investigate if inflammation-driven iron dyshomeostasis exacerbates post-stroke recovery impairment.
  • To elucidate the underlying molecular mechanisms connecting iron metabolism and stroke recovery.

Main Methods:

  • Utilized Ferroportin 1 (FPN1) deficient mice (Fpn1Nestin-CKO) to model neuronal and glial FPN1 deficiency.
  • Assessed sensorimotor function recovery, neuronal injury, apoptosis, necroptosis, myelin and synapse repair, and dendritic spine density.
  • Conducted histological analyses (H&E, Nissl), IgG extravasation assays, and measured iron metabolism-related molecules and inflammatory cytokines.
  • Investigated the effect of JAK-STAT signaling inhibition (AG490) on iron homeostasis and repair pathways.

Main Results:

  • FPN1 deficiency significantly delayed sensorimotor recovery and worsened neuronal injury, apoptosis, and necroptosis.
  • Impaired myelin/synapse repair and reduced dendritic spine density were observed in FPN1-deficient mice.
  • Increased iron accumulation, elevated inflammatory cytokines, hepcidin levels, and blood-brain barrier (BBB) disruption were noted in the ischemic cortex.
  • JAK-STAT inhibition modulated iron and repair responses, with greater effects in FPN1-deficient mice.

Conclusions:

  • Inflammatory signaling, BBB dysfunction, and iron dyshomeostasis are closely interconnected in post-stroke recovery.
  • Neuronal and glial FPN1 deficiency contributes to delayed recovery via inflammation-induced BBB disruption and iron accumulation.
  • Targeting iron metabolism and inflammatory pathways presents a potential therapeutic strategy for stroke recovery.