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  4. Role of CD36 in central nervous system diseases

Role of CD36 in central nervous system diseases

Neural Regeneration Research, 2024 · DOI: https://doi.org/10.4103/1673-5374.380821 · Published: March 1, 2024

PharmacologyNeurology

Simple Explanation

CD36, a protein found in the nervous system, is involved in processes that worsen central nervous system diseases like stroke and Alzheimer's. Targeting CD36 with antagonists could provide new treatment strategies. CD36 dysregulation is related to Parkinson’s disease (PD), stroke, Alzheimer’s disease (AD), and other neurological diseases. CD36 is involved in mediating endothelial dysfunction, oxidative stress, mitochondrial dysfunction, and inflammatory responses, which can accelerate neurodegenerative processes and cognitive decline. The review explores the mechanisms of action of CD36 antagonists, such as Salvianolic acid B, tanshinone IIA, curcumin, sulfosuccinimidyl oleate, antioxidants, and small-molecule compounds. Moreover, the structures of binding sites between CD36 and antagonists were predicted.

Study Duration
From 2017 to 2022
Participants
Animal models
Evidence Level
Review article

Key Findings

  • 1
    CD36 mediates endothelial dysfunction, oxidative stress, mitochondrial dysfunction, and inflammatory responses, contributing to CNS diseases.
  • 2
    CD36 antagonists like Salvianolic acid B, tanshinone IIA, and curcumin show promise in inhibiting CD36-mediated pathways.
  • 3
    Molecular docking predictions suggest specific binding sites between CD36 and antagonists, offering targets for drug development.

Research Summary

This review focuses on the role of CD36, a scavenger receptor, in central nervous system (CNS) diseases and explores potential therapeutic strategies involving CD36 antagonists. The review discusses the mechanisms of action of various CD36 antagonists, including Salvianolic acid B, tanshinone IIA, curcumin, and sulfosuccinimidyl oleate, and predicts the structures of binding sites between CD36 and these antagonists. It concludes that CD36 mediates several risk factors associated with CNS diseases, suggesting that further research is needed to investigate the exact mechanisms of CD36 action and the ideal administration times of CD36 antagonists in diverse disorders.

Practical Implications

Drug Development

The identification of CD36 as a therapeutic target and the exploration of various CD36 antagonists can lead to the development of new and more effective treatments for CNS diseases.

Clinical Strategies

Understanding the mechanisms of CD36 action in various disorders can help in devising better clinical strategies for managing and treating CNS diseases.

Personalized Medicine

Identifying specific binding sites between CD36 and antagonists can pave the way for developing personalized medicine approaches targeting CD36 in CNS diseases.

Study Limitations

  • 1
    More neurological disease trials are needed to elucidate the exact mechanisms of CD36 in CNS disease.
  • 2
    Most of the studies cited are from animal models, while clinical trials are not abundant.
  • 3
    Further comprehensive clinical trials are needed to elucidate the role of CD36 in CNS disorders.

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