Exercise training and dietary restriction affect PINK1/Parkin and Bnip3/Nix-mediated cardiac mitophagy in mice

Zhao, Yungang; Zhu, Qiaodi; Song, Wenjuan; Gao, Beibei

doi:10.4149/gpb_2018020

Cited by 11 publications

(14 citation statements)

References 36 publications

(44 reference statements)

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“…Nix, as a protein of autophagy receptor, recruits members of the Atg8 family to the injured mitochondria through its own LIR motifs, thereby resulting in the removal of the mitochondria (Schwarten et al, 2009). Secondly, the PINK1/Parkin pathway is a significant pathway mediating mitophagy, and the activation of this pathway is associated with a decrease in the membrane potential of mitochondria (Zhao et al, 2018). Some studies have shown that high expression of Nix can induce a decrease of the mitochondrial membrane potential, and then activate the PINK1/Parkin pathway to co-mediated mitophagy (McLelland et al, 2014;Gao et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Nix Plays a Neuroprotective Role in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

et al. 2020

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Nix is located in the outer membrane of mitochondria, mediates mitochondrial fission and implicated in many neurological diseases. However, the association between Nix and subarachnoid hemorrhage (SAH) has not previously been reported. Therefore, the present study was designed to evaluate the expression of Nix and its role in early brain injury (EBI) after SAH. Adult male Sprague-Dawley (SD) rats were randomly assigned to various time points for investigation after SAH. A rat model of SAH was induced by injecting 0.3 ml of autologous non-heparinized arterial blood into the prechiasmatic cistern. The expression of Nix was investigated by Western blot and immunohistochemistry. Next, Nix-specific overexpression plasmids and small interfering RNAs (siRNAs) were separately administered. Western blot, neurological scoring, Morris water maze, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and fluoro-jade B (FJB) staining were performed to evaluate the role of Nix in EBI following SAH. We found that Nix was expressed in neurons and its expression level in the SAH groups was higher than that in the Sham group, which peaked at 24 h after SAH. Overexpression of Nix following SAH significantly decreased the expression of translocase of outer mitochondrial membrane 20 (TOMM20, a marker of mitochondria), ameliorated neurological/cognitive deficits induced by SAH, and reduced the total number of apoptotic/neurodegenerative cells, whereas siRNA knockdown of Nix yielded opposite effects. Taken together, our findings demonstrated that the expression of Nix is increased in neurons after experimental SAH in rats, and may play a neuroprotective role in EBI following SAH.

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Section: Discussionmentioning

confidence: 99%

Nix Plays a Neuroprotective Role in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

et al. 2020

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“…It is possible that the parameters of the exercise paradigm used in this study were not rigorous enough to exacerbate similar cardiovascular changes in PinK1 KO rats. There also is evidence that augmented mitochondrial function plays a role in exercise-related changes in mitophagy in cardiac tissue [73,74]…”

Section: U N C O R R E C T E D a U T H O R P R O O Fmentioning

confidence: 99%

Establishing Equivalent Aerobic Exercise Parameters Between Early-Stage Parkinson’s Disease and Pink1 Knockout Rats

Salvatore

Soto

Kasanga

et al. 2022

JPD

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Background: Rodent Parkinson’s disease (PD) models are valuable to interrogate neurobiological mechanisms of exercise that mitigate motor impairment. Translating these mechanisms to human PD must account for physical capabilities of the patient. Objective: To establish cardiovascular parameters as a common metric for cross-species translation of aerobic exercise impact. Method: We evaluated aerobic exercise impact on heart rate (HR) in 21 early-stage PD subjects (Hoehn Yahr ≤1.5) exercising in non-contact boxing training for ≥3 months, ≥3x/week. In 4-month-old Pink1 knockout (KO) rats exercising in a progressively-increased treadmill speed regimen, we determined a specific treadmill speed that increased HR to an extent similar in human subjects. Results: After completing aerobic exercise for ∼30 min, PD subjects had increased HR∼35% above baseline (∼63% maximum HR). Motor and cognitive test results indicated the exercising subjects completed the timed up and go (TUG) and trail-making test (TMT-A) in significantly less time versus exercise-naïve PD subjects. In KO and age-matched wild-type (WT) rats, treadmill speeds of 8–10 m/min increased HR up to 25% above baseline (∼67% maximum HR), with no further increases up to 16 m/min. Exercised KO, but not WT, rats showed increased locomotor activity compared to an age-matched exercise-naïve cohort at 5 months old. Conclusion: These proof-of-concept results indicate HR is a cross-species translation parameter to evaluate aerobic exercise impact on specific motor or cognitive functions in human subjects and rat PD models. Moreover, a moderate intensity exercise regimen is within the physical abilities of early-stage PD patients and is therefore applicable for interrogating neurobiological mechanisms in rat PD models.

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“…Bnip3 expression was significantly upregulated in the CR rat kidneys, suggesting mitophagy can be increased by CR while the expression of Binp3 decreased in high‐caloric condition that indicated possibility of preventing mitophagy in this condition. In another study, Zhao et al 52 . examined the effects of exercise training and DR on cardiac mitophagy.…”

Section: Resultsmentioning

confidence: 99%

“…Bnip3 expression was significantly upregulated in the CR rat kidneys, suggesting mitophagy can be increased by CR while the expression of Binp3 decreased in high-caloric condition that indicated possibility of preventing mitophagy in this condition. In another study, Zhao et al 52 examined the effects of exercise training and DR on cardiac mitophagy. Eight-week-old male mice were given AL water and standard mouse food before being randomly allocated in one of three groups; control (nÀ8), exercise trained (n = 8, mice underwent swim training 5 days/week for 10 weeks), CR (n = 8 mice were fed 40% less calories than normal for 10 weeks), and exercise training + CR (T + CR) groups.…”

Section: Fasting or Calorie Restriction And Mitophagymentioning

confidence: 99%

The effect of fasting or calorie restriction on mitophagy induction: a literature review

Mehrabani

Bagherniya

Askari

et al. 2020

J cachexia sarcopenia muscle

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Mitochondrial dysfunction can be a major cause of a wide range of age-related diseases. Maintaining the normal homeostasis of mitochondria population plays an important role in ensuring people's health, which is done through the mitophagy process. Among the various stimuli for the onset of mitophagy, caloric restriction (CR) is one of the strongest non-genetic triggers for initiating the mitophagy process. The primary objective of this paper is to review the literature assessing the effect of CR on mitophagy. Medline, Web of Science, Scopus, and Google Scholar databases was searched from inception to 1 August 2019. Reference lists from all selected articles were also examined for additional relevant studies. The evidence regarding the effect of fasting or CR on mitophagy is still limited. In addition, the methodological approaches of the studies are too heterogeneous in terms of types of food restriction, study duration, and targeted tissues. Most of the studies showed that fasting or CR induced mitophagy and mitophagy-related markers such as Binp3 and Parkin. However, some studies demonstrated that mitophagy occurred both in fasting and fed state with no significant differences or may be induced in fed state. Study on the muscle tissue of subjects after exercise showed that mitophagy was upregulated in the fed state. It has been demonstrated that mitophagy in the muscle was lowered in the absence of AMP-dependent kinase and fibroblast growth factor 21 genes, both in fasted and fed conditions. Current evidence overwhelmingly suggests that CR and fasting induce mitophagy and mitophagy-related markers. Based on the current evidence that we reviewed here, it could be concluded that fasting or CR has a promising role as a novel and practical approach in the prevention of age-related diseases without any side effects by inducing mitophagy in different organs of the body. More studies will be required in future to clarify the relationship between food deprivation and mitophagy. Further studies using a variety of different types of CR and fasting states are also warranted to determine the best approach for inducing mitophagy and improving health.

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Exercise training and dietary restriction affect PINK1/Parkin and Bnip3/Nix-mediated cardiac mitophagy in mice

Cited by 11 publications

References 36 publications

Nix Plays a Neuroprotective Role in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

Nix Plays a Neuroprotective Role in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats

Establishing Equivalent Aerobic Exercise Parameters Between Early-Stage Parkinson’s Disease and Pink1 Knockout Rats

The effect of fasting or calorie restriction on mitophagy induction: a literature review

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