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Publications

Journal Article Review Epublish 1 citation

PubMed: 37534043 DOI: 10.3389/fncel.2023.1193362

Potential enhancement of post-stroke angiogenic response by targeting the oligomeric aggregation of p53 protein.

Front Cell Neurosci 17:1193362

Authors: Hoi Hei Tam, Dongxing Zhu, Samuel Sze King Ho, Heng Wai Vong, Vincent Kam Wai Wong, Simon Wing-Fai Mok, Io Nam Wong

Affiliations

  • Faculty of Medicine, Macau University of Science and Technology, Macau, Macau SAR, China.
  • Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
  • Dr. Neher's Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, Macau SAR, China.
  • Faculty of Medicine, Macau University of Science and Technology, Macau, Macau SAR, China. Dr. Neher's Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, Macau SAR, China.

Abstract

Tumor suppressor gene p53 and its aggregate have been found to be involved in many angiogenesis-related pathways. We explored the possible p53 aggregation formation mechanisms commonly occur after ischemic stroke, such as hypoxia and the presence of reactive oxygen species (ROS). The angiogenic pathways involving p53 mainly occur in nucleus or cytoplasm, with one exception that occurs in mitochondria. Considering the high mitochondrial density in brain and endothelial cells, we proposed that the cyclophilin D (CypD)-dependent vascular endothelial cell (VECs) necrosis pathway occurring in the mitochondria is one of the major factors that affects angiogenesis. Hence, targeting p53 aggregation, a key intermediate in the pathway, could be an alternative therapeutic target for post-stroke management.

MeSH

Stroke, Genes, P53, Mitochondria, Endothelial Cells