BNIP3L/NIX-mediated mitophagy alleviates passive stress-coping behaviors induced by tumor necrosis factor-α

Lu, Jia-Jing; Wu, Pengfei; He, Jin-Gang; Li, Yuke; Long, Li‐Hong; Yao, Xia-Ping; Yang, Jia-Hao; Chen, Hongsheng; Zhang, Xiang-Nan; Hu, Zhuang-Li; Chen, Zhong; Wang, Fang; Chen, Jianguo

doi:10.1038/s41380-023-02008-z

Cited by 13 publications

(6 citation statements)

References 86 publications

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“…Notably, NIX protein expression was prominently lower in the CUMS group compared to controls, whereas no differences were observed for Parkin protein (Jin et al, 2023). Similarly, the mRNA expression of NIX and LC3A was downregulated in the blood of mice induced by LPS and CSDS, while OPTN and NDP52 proteins remained unaffected in CSDS (Lu et al, 2023).…”

Section: Impaired Mitophagy In Mdd Modelsmentioning

confidence: 87%

“…Patients with depression might experience impaired mitochondria clearance, seen through higher PINK1, P62, and LC3B levels in peripheral blood nuclear cells, and lower Parkin levels (Scaini et al, 2022). The mRNA levels of PINK1, NIX, and LC3A were significantly lower in the blood of MDD patients (Weixing, 2019;Lu et al, 2023). The 18 kDa translocator protein (TSPO) has gained increased attention for its role as a crucial rate-limiting step in neurosteroidogenesis and its potential implications in the pathophysiology of stress response and related disorders (Beurdeley- Thomas et al, 2000;Pinna and Rasmusson, 2012).…”

Section: Impaired Mitophagy In Mdd Patientsmentioning

confidence: 99%

“…Fluoxetine, a pioneer of the SSRI class, has gained widespread used for its significant clinical efficacy and favorable safety profile (Perez-Caballero et al, 2014;Micheli et al, 2018;Shu et al, 2019;Hetrick et al, 2021). In a study involving CUMS-induced mice, fluoxetine was found to enhance NIX-mediated mitophagy by reducing the LC3BII/I and P62 expression while increasing NIX expression, without affecting Parkin levels (Lu et al, 2023). Additionally, the level of mitophagy was promoted by regulating the levels of mitophagy-related proteins such as TSPO, VDAC1, PINK1, and Beclin-1 in LH mice brains.…”

Section: The Effect Of Classic Antidepressants On Mitophagymentioning

confidence: 99%

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Targeting mitophagy for depression amelioration: a novel therapeutic strategy

Xu,

Gao,

Guo

et al. 2023

Front. Neurosci.

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Major depressive disorder is a global psychiatric condition characterized by persistent low mood and anhedonia, which seriously jeopardizes the physical and mental well-being of affected individuals. While various hypotheses have been proposed to explicate the etiology of depression, the precise pathogenesis and effective treatment of this disorder remain elusive. Mitochondria, as the primary organelles responsible for cellular energy production, possess the ability to meet the essential energy demands of the brain. Research indicated that the accumulation of damaged mitochondria is associated with the onset of depression. Mitophagy, a type of cellular autophagy, specifically targets and removes excess or damaged mitochondria. Emerging evidence demonstrated that mitophagy dysfunction was involved in the progression of depression, and several pharmacological interventions that stimulating mitophagy exerted excellent antidepressant actions. We provided an overview of updated advancements on the regulatory mechanism of mitophagy and the mitophagy abnormality in depressed patients and animals, as well as in cell models of depression. Meanwhile, various therapeutic strategies to restore mitophagy for depression alleviation were also discussed in this review.

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Section: Impaired Mitophagy In Mdd Modelsmentioning

confidence: 87%

Section: Impaired Mitophagy In Mdd Patientsmentioning

confidence: 99%

Section: The Effect Of Classic Antidepressants On Mitophagymentioning

confidence: 99%

See 1 more Smart Citation

Targeting mitophagy for depression amelioration: a novel therapeutic strategy

Xu,

Gao,

Guo

et al. 2023

Front. Neurosci.

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“…In mitophagy, previous studies have shown that fluoxetine increases the expression of NIX and enhances NIX‐mediated mitophagy in the hippocampus of CUMS mice 65,66 . Notably, Ketamine, a rapid on‐set and long‐lasting antidepressant, particularly in patients with treatment‐resistant depression, reverses the TNF‐α‐induced behavior despair through activation of NIX‐mediated mitophagy in the medial prefrontal cortex 101 . Interestingly, Oridonin, the major active ingredient of the traditional Chinese medicinal herb Rabdosia rubescens, enhances mitophagy in LPS‐treated hippocampal astrocytes and attenuates cell death caused by ROS accumulation, 102 which has been considered as one of the important causes of depression.…”

Section: Antidepressants and Mitochondriamentioning

confidence: 99%

“…65,66 Notably, Ketamine, a rapid on-set and long-lasting antidepressant, particularly in patients with treatment-resistant depression, reverses the TNFα-induced behavior despair through activation of NIX-mediated mitophagy in the medial prefrontal cortex. 101 Interestingly, Oridonin, the major active ingredient of the traditional Chinese medicinal herb Rabdosia rubescens, enhances mitophagy in LPS-treated hippocampal astrocytes and attenuates cell death caused by ROS accumulation, 102 which has been considered as one of the important causes of depression. Additionally, as for the mitochondrial fusion and fission, Suwanjang et al 103 demonstrated that Spilanthes acmella Murr.…”

Section: Antidepressants Amend the Mitochondrial Quality Control Systemsmentioning

confidence: 99%

Mitochondria in depression: The dysfunction of mitochondrial energy metabolism and quality control systems

Jiang,

Wang,

Sheng

2024

CNS Neurosci Ther

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BackgroundDepression is the most disabling neuropsychiatric disorder, causing difficulties in daily life activities and social interactions. The exact mechanisms of depression remain largely unclear. However, some studies have shown that mitochondrial dysfunction would play a crucial role in the occurrence and development of depression.AimsTo summarize the known knowledge about the role of mitochondrial dysfunction in the pathogenesis of depression.MethodsWe review the recent literature， including 105 articles, to summarize the mitochondrial energy metabolism and quality control systems in the occurrence and development of depression. Some antidepressants which may exert their effects by improving mitochondrial function are also discussed.ResultsImpaired brain energy metabolism and (or) damaged mitochondrial quality control systems have been reported not only in depression patients but in animal models of depression. Although the classical antidepressants have not been specially designed to target mitochondria, the evidence suggests that many antidepressants may exert their effects by improving mitochondrial function.ConclusionsThis brief review focuses on the findings that implicate mitochondrial dysfunction and the quality control systems as important etiological factors in the context of depressive disorders. It will help us to understand the various concepts of mitochondrial dysfunction in the pathogenesis of depression, and to explore novel and more targeted therapeutic approaches for depression.

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MT-TN mutations lead to progressive mitochondrial encephalopathy and promotes mitophagy

Duan,

Pan,

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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BNIP3L/NIX-mediated mitophagy alleviates passive stress-coping behaviors induced by tumor necrosis factor-α

Cited by 13 publications

References 86 publications

Targeting mitophagy for depression amelioration: a novel therapeutic strategy

Targeting mitophagy for depression amelioration: a novel therapeutic strategy

Mitochondria in depression: The dysfunction of mitochondrial energy metabolism and quality control systems

MT-TN mutations lead to progressive mitochondrial encephalopathy and promotes mitophagy

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