Sestrin/FNDC5: An ancient axis connecting exercise and thermoregulation

Wessells, Robert J.; Lee, Junhee

doi:10.1111/apha.13804

Cited by 3 publications

(2 citation statements)

References 8 publications

(23 reference statements)

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“…Sestrin2 was also important for mediating exercise effects in other organs. For instance, Sestrin2 loss attenuated the exercise-induced browning of white adipose tissue in mice [55,56]. This was thought to be mediated through increased production of Irisin/FNDC5, which could be induced by Sestrin2 through the AMPK-PGC1 axis.…”

Section: The Role Of Sestrins In Exercise Adaptation and Benefitsmentioning

confidence: 99%

Muscular Sestrins: Roles in Exercise Physiology and Stress Resistance

Hwang

Kim

2023

Biomolecules

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Sestrins are a family of stress-inducible proteins that are critical for stress adaptation and the maintenance of metabolic homeostasis. High expression of Sestrins is observed in skeletal and cardiac muscle tissues, suggesting their significance in the physiological homeostasis of these organs. Furthermore, expression of Sestrins is dynamically controlled in the tissues, based on the level of physical activity and the presence or absence of stress insults. Genetic studies in model organisms have shown that muscular Sestrin expression is critical for metabolic homeostasis, exercise adaptation, stress resistance, and repair and may mediate the beneficial effects of some available therapeutics. The current minireview summarizes and discusses recent findings that shed light on the role of Sestrins in regulating muscle physiology and homeostasis.

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Section: The Role Of Sestrins In Exercise Adaptation and Benefitsmentioning

confidence: 99%

Muscular Sestrins: Roles in Exercise Physiology and Stress Resistance

Hwang

Kim

2023

Biomolecules

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“…Increased SESN1 expression was found in neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R) treatment, and silencing of SESN1 makes neurons more susceptible to OGD/R damage, and upregulation of SESN1 improves OGD/R-induced neuronal damage by reducing apoptosis and production of ROS [13]. However, the possible effects of Sestrin on POCD were still unclear.…”

Section: Introductionmentioning

confidence: 99%

SESN1, as a potential target for postoperative cognitive dysfunction, attenuates sevoflurane-induced neuronal cell damage in the hippocampus

2023

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Postoperative cognitive dysfunction (POCD) is a devastating complication with long-term consequences, and new therapeutic targets and drugs are still needed for the treatment of POCD. Sestrin are a family of stress-inducing proteins that regulate cellular metabolic networks. However, the possible effects of Sestrin on POCD were still unclear. This study aimed to investigate the effects of Sestrin 1 (SESN1) in postoperative cognitive dysfunction (POCD) cell model and reveal its mechanism. We constructed an in vitro model of POCD by treating primary rat hippocampal neurons with sevoflurane. Herein, we noticed SESN1 enhanced cell viability induced by sevoflurane. Further, SESN1 improved sevoflurane-induced cell inflammation. We further found that SESN1 improved sevoflurane induced reactive oxygen species (ROS) production and inhibited apoptosis. Mechanically, SESN1 restrained NOD-like receptor thermal protein domain 3 (NLRP3) inflammasome activation and therefore suppressed POCD. In conclusion, SESN1, as a potential target for postoperative cognitive dysfunction, attenuates sevoflurane-induced neuronal cell damage in the hippocampus. These findings will provide guidance for the mechanism study of POCD and future drug development for treatment of POCD.

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