中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (5): 984-985.doi: 10.4103/1673-5374.297072

• 观点:退行性病与再生 • 上一篇    下一篇

核过氧化物酶体增殖物激活受体γ可作为治疗滥用药物引起的神经退变和依赖性的治疗靶标

  

  • 出版日期:2021-05-15 发布日期:2020-12-29

Nuclear peroxisome proliferator activated receptor-gamma (PPARγ) as a therapeutic target to treat neurodegeneration and dependence elicited by drugs of abuse

Roberto Ciccocioppo*, Massimo Ubaldi   

  1. School of Pharmacy, Pharmacology Unit, University of Camerino, Camerino, Italy
  • Online:2021-05-15 Published:2020-12-29
  • Contact: Roberto Ciccocioppo, roberto.ciccocioppo@unicam.it.

摘要: https://orcid.org/0000-0003-3126-9240 (Roberto Ciccocioppo) 

Abstract: Peroxisome proliferator activated receptors (PPARs) are ligand-activated transcription factors that are located in the cytoplasm. After activation by specific ligands, PPARs enter the nucleus and heterodimerize with the retinoid x receptor. This heterodimer binds to PPAR response element in DNA to regulate the transcription of genes that are involved in different physiological processes, including insulin sensitization, inflammatory response, and neuroprotection (Kapadia et al., 2008). The PPAR receptor family is composed of three isoforms—PPARα, PPARδ and PPARγ—that are expressed in both peripheral tissues and the brain. Endogeneous ligands of PPARγ include polyunsatured fatty acids (e.g., oleic acid and arachidonic acid), prostaglandins, and low-density lipoproteins. PPARγ can also be targeted by specific synthetic agonists that belong to the class of thiazolidinediones (TZDs), including pioglitazone and rosiglitazone. Because of their ability to bind PPARγ, TZDs are approved for the treatment of type 2 diabetes and insulin resistance, improving insulin sensitivity in muscle, liver, and adipose tissue.