Abstract
Mitochondrion is a multi-functional organelle, which is associated with various signaling pathway networks, including energy metabolism, oxidative stress, cell apoptosis, cell cycles, autophagy, and immunity process. Mitochondrial proteins have been discovered to modulate these signaling pathway networks, and multiple biological behaviors to adapt to various internal environments or signaling events of human pathogenesis. Accordingly, mitochondrial dysfunction that alters the bioenergetic and biosynthetic state might contribute to multiple diseases, including cell transformation and tumor. Multiomics studies have revealed that mitochondrial dysfunction, oxidative stress, and cell cycle dysregulation signaling pathways operate in human pituitary adenomas, which suggest mitochondria play critical roles in pituitary adenomas. Some drugs targeting mitochondria are found as a therapeutic strategy for pituitary adenomas, including melatonin, melatonin inhibitors, temozolomide, pyrimethamine, 18 beta-glycyrrhetinic acid, gossypol acetate, Yougui pill, T-2 toxin, grifolic acid, cyclosporine A, dopamine agonists, and paeoniflorin. This article reviews the latest experimental evidence and potential biological roles of mitochondrial dysfunction and mitochondrial dynamics in pituitary adenoma progression, potential molecular mechanisms between mitochondria and pituitary adenoma progression, and current status and perspectives of mitochondria-based biomarkers and targeted drugs for effective management of pituitary adenomas.
Highlights
Pituitary adenomas are intracranial tumors that develop in the pituitary gland, and account for 10 to 25% of all intracranial neoplasms
The density of infiltrated CD4+ and CD8+ T-lymphocytes may be relatively insufficient in these pituitary adenomas, but CD4+ and CD8+ T lymphocytes are significantly more in Growth hormone (GH)-secreting adenomas than non-GH adenomas. Both densely and sparsely granulated GH-adenomas had significantly more CD4+ cells than adrenocorticotrophic hormone (ACTH)-adenomas, and significantly more CD8+ cells than null cell adenomas. These results suggest an association of the enhanced T-lymphocytes infiltration and invasiveness in pituitary adenomas, and that adjuvant immunotherapy might block the tumor enlargement and invasiveness of pituitary adenomas [129]
Several lines of evidence indicate that mitochondrial dysfunction emerge cross-links with various complex biological processes, including energy metabolism, oxidative stress, cell apoptosis, cell cycle, mitophagy, and immunity process
Summary
Pituitary adenomas are intracranial tumors that develop in the pituitary gland, and account for 10 to 25% of all intracranial neoplasms. Mitochondria are center of oxidative stress, which clearly demonstrate that mitochondrial dysfunction pathway plays important roles in pituitary adenomas. This review article discusses observations in the context of how mitochondrial dysfunction can influence the biological status in pituitary adenoma, including energy metabolism, oxidative stress, cell apoptosis, autophagy, and immunity (Figure 1; Table 2).
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