2023
DOI: 10.1038/s41419-023-05676-5
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Melatonin-mediated FKBP4 downregulation protects against stress-induced neuronal mitochondria dysfunctions by blocking nuclear translocation of GR

Abstract: The physiological crosstalk between glucocorticoid and melatonin maintains neuronal homeostasis in regulating circadian rhythms. However, the stress-inducing level of glucocorticoid triggers mitochondrial dysfunction including defective mitophagy by increasing the activity of glucocorticoid receptors (GRs), leading to neuronal cell death. Melatonin then suppresses glucocorticoid-induced stress-responsive neurodegeneration; however, the regulatory mechanism of melatonin, i.e., associated proteins involved in GR… Show more

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Cited by 8 publications
(9 citation statements)
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“…Proteome analysis of the locus coeruleus in PD patients revealed downregulated levels of FKBP4 [ 41 ]. Kim et al highlighted the protective effect of melatonin-mediated downregulation of FKBP4 on neuronal mitochondria dysfunctions [ 42 ]. While FKBP4 is recognized for its involvement in diverse cellular processes beyond immunosuppression, further exploration is essential to understand its role in PD pathology.…”
Section: Discussionmentioning
confidence: 99%
“…Proteome analysis of the locus coeruleus in PD patients revealed downregulated levels of FKBP4 [ 41 ]. Kim et al highlighted the protective effect of melatonin-mediated downregulation of FKBP4 on neuronal mitochondria dysfunctions [ 42 ]. While FKBP4 is recognized for its involvement in diverse cellular processes beyond immunosuppression, further exploration is essential to understand its role in PD pathology.…”
Section: Discussionmentioning
confidence: 99%
“…A plethora of data show melatonin [ 58 , 59 ], including indirectly [ 60 , 61 ] to modulate all immune cells, although seldom are the interactions of melatonin and GR activation investigated in immune cells. In studies investigating GR and melatonin interactions, it is clear that melatonin significantly modulates GR effects, including via FKBP4 regulation [ 62 ], as shown in immune cells [ 45 ]. It is widely recognized that glucocorticoid treatments, by suppressing NK cells and cytolytic cells, enhances cancer pathogenesis [ 61 ], thereby linking to how stress induced HPA axis activation and glucocorticoid treatment increase cancer susceptibility and modulate progression [ 63 ].…”
Section: Aging Cancer Susceptibility Pineal Melatonin and Cortisolmentioning
confidence: 99%
“…Importantly, the different cells of the immune system have long been recognized to be differentially regulated by the circadian rhythm [57]. A plethora of data show melatonin [58,59], including indirectly [60,61] to modulate all immune cells, although seldom are the interactions of melatonin and GR activation investigated in immune cells. In studies investigating GR and melatonin interactions, it is clear that melatonin significantly modulates GR effects, including via FKBP4 regulation [62], as shown in immune cells [45].…”
Section: Aging Cancer Susceptibility Pineal Melatonin and Cortisolmentioning
confidence: 99%
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“… 2 The circadian hormone melatonin, which can antagonize GR translocation, may alleviate the effect of stress and demonstrate effectiveness in IBS patients. 11 , 12 In addition, GR interacts with enhancer GREs and the cohesin loader nipped-B-like protein (NIPBL) to initiate chromatin loop extrusion as a mechanism for long-distance regulation: GR and NIPBL bind enhancer GREs firstly and load cohesin ring to guide the formation of chromatin loop, then the chromatin slides through the cohesin ring until the formation of stable transcription-regulatory enhancer-promoter interaction via the TF binding DNA elements. 13 E-box is a DNA response element targeted by the CLOCK:BMAL1 TF complex in the circadian transcriptional network.…”
Section: Introductionmentioning
confidence: 99%