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Related Concept Videos

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.
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...

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Gain-of-function PPM1D mutations attenuate ischemic stroke.

Wenyan He1, Yan Li1, Junwan Fan1

  • 1Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Beijing Key Laboratory of innovative Drug and Device Research & Development for Cerebrovascular Diseases, Beijing, China.

Cell Death and Differentiation
|May 21, 2025
PubMed
Summary
This summary is machine-generated.

Genetic mutations in the protein phosphatase magnesium-dependent 1 delta (PPM1D) gene protect against ischemic stroke. A novel drug, T2755, stabilizes PPM1D and shows promise for treating stroke.

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Area of Science:

  • Genetics
  • Neurology
  • Pharmacology

Background:

  • Stroke is a leading cause of death globally, necessitating research into its genetic underpinnings and therapeutic strategies.
  • Identifying genetic factors influencing stroke pathogenesis is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of genetic aberrations, specifically in the PPM1D gene, in the context of ischemic stroke.
  • To explore the therapeutic potential of targeting PPM1D for stroke treatment.

Main Methods:

  • Whole-genome sequencing of 10,241 ischemic stroke patients.
  • Analysis of PPM1D mutations and their association with clinical phenotypes.
  • Experimental induction of brain ischemia in Ppm1d-deficient mice.
  • Spatial transcriptomics and proteomic analysis of brain endothelial cells.
  • Identification and validation of a PPM1D stabilizing small molecule (T2755).

Main Results:

  • Eight patients with gain-of-function PPM1D mutations showed improved clinical outcomes and reduced inflammation markers.
  • Ppm1d-deficient mice exhibited worsened stroke outcomes, including larger lesions and neurological deficits.
  • PPM1D deficiency disrupted endothelial homeostasis and fatty acid metabolism via the PPARα pathway.
  • The small molecule T2755 stabilized PPM1D and significantly reduced ischemic brain injury in mice.

Conclusions:

  • Gain-of-function mutations in PPM1D confer protection against ischemic brain injury.
  • PPM1D plays a critical role in maintaining endothelial homeostasis during ischemic stroke.
  • Pharmacological stabilization of PPM1D using T2755 represents a promising therapeutic approach for ischemic stroke.