Single bout of running exercise changes LC3-II expression in rat cardiac muscle

Ogura, Yuji; Iemitsu, Motoyuki; Naito, Hisashi; Kakigi, Ryo; Kakehashi, Chiaki; Maeda, Seiji; Akema, Tatsuo

doi:10.1016/j.bbrc.2011.09.152

Cited by 57 publications

(46 citation statements)

References 28 publications

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“…AEE promotes cardiac autophagy that reaches its maximum between 30 and 80 min after exercise (12,23). Consistent with these data, our results also reveal that a single bout of endurance exercise enhances cardiac autophagy 1 h after exercise.…”

Section: Discussionsupporting

confidence: 92%

“…As reported from a study of He et al (12), our study shows that the kinetophagy is not just due to accumulation of autophagosomes but also due to augmented autophagic flux, evidenced by both increased LC3-II levels and LC3-II/LC3-I ratio and decreased p62 levels. Contrary to our observation, Ogura et al (23) failed to show an increase in autophagy flux (no changes in p62) despite the similar exercise protocol. Furthermore, a study from Quindry et al (26) and others using rats have reported that neither three consecutive days nor 36 wk of treadmill running (1) does not modulate autophagy levels (i.e, Beclin-1 and LC3-II/LC3-I ratio).…”

Section: Discussioncontrasting

confidence: 78%

“…Furthermore, a study from Quindry et al (26) and others using rats have reported that neither three consecutive days nor 36 wk of treadmill running (1) does not modulate autophagy levels (i.e, Beclin-1 and LC3-II/LC3-I ratio). Although very little is known about how exercise modulates autophagy, it can be presumed that autophagy by endurance exercise may be an early adaptive response; for example, studies showed that an autophagic response declines fairly quickly (approximately 60-80 min after exercise) (12,23). Thus, measuring time points of autophagy may yield variable results.…”

Section: Discussionmentioning

confidence: 95%

“…Notably, recent evidence has shown that acute endurance exercise (AEE) is a potent inducer of autophagy (12,23) in skeletal muscles and the heart. However, the cellular and molecular mechanisms of exercise-mediated autophagy remain to be elucidated.…”

mentioning

confidence: 99%

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Cardiac Kinetophagy Coincides with Activation of Anabolic Signaling

Lee

Kang

Kwon

et al. 2016

Medicine &Amp; Science in Sports &Amp; Exercise

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Section: Discussionsupporting

confidence: 92%

Section: Discussioncontrasting

confidence: 78%

Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

See 2 more Smart Citations

Cardiac Kinetophagy Coincides with Activation of Anabolic Signaling

Lee

Kang

Kwon

et al. 2016

Medicine &Amp; Science in Sports &Amp; Exercise

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“…Deeper investigation into these apparent 'exceptions to the rule' might prove particularly fruitful. For example, exercise induces both autophagy and cell growth of muscle fibers (Ogura et al, 2011), and this might involve a temporal separation into distinct phases of fiber breakdown and rebuilding. Similarly, senescent cells display high levels of autophagy despite showing highly active mTOR signaling and protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

Autophagy and cell growth – the yin and yang of nutrient responses

Neufeld

2012

Journal of Cell Science

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SummaryAs a response to nutrient deprivation and other cell stresses, autophagy is often induced in the context of reduced or arrested cell growth. A plethora of signaling molecules and pathways have been shown to have opposing effects on cell growth and autophagy, and results of recent functional screens on a genomic scale support the idea that these processes might represent mutually exclusive cell fates. Understanding the ways in which autophagy and cell growth relate to one another is becoming increasingly important, as new roles for autophagy in tumorigenesis and other growth-related phenomena are uncovered. This Commentary highlights recent findings that link autophagy and cell growth, and explores the mechanisms underlying these connections and their implications for cell physiology and survival. Autophagy and cell growth can inhibit one another through a variety of direct and indirect mechanisms, and can be independently regulated by common signaling pathways. The central role of the mammalian target of rapamycin (mTOR) pathway in regulating both autophagy and cell growth exemplifies one such mechanism. In addition, mTOR-independent signaling and other more direct connections between autophagy and cell growth will also be discussed.This article is part of a Minifocus on Autophagy. For further reading, please see related articles: 'Ubiquitin-like proteins and autophagy at a glance' by Tomer Shpilka et al. (J. Cell Sci. 125, 2343-2348 and 'Autophagy and cancer -issues we need to digest' by Emma Liu and Kevin Ryan (J. Cell Sci. 125, 2349-2358).

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Autophagy as a Potential Target for Sarcopenia

et al. 2015

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Sarcopenia is an aging-related disease with a significant reduction in mass and strength of skeletal muscle due to the imbalance between protein synthesis and protein degradation. The loss of skeletal muscle is an inevitable event during aging process, which can result in the significant impact on the quality of life, and also can increase the risk for other aging-associated diseases in the elderly. However, the underlying molecular mechanism of aging-related skeletal muscle loss is still poorly understood. Autophagy is a degradation pathway for the clearance of dysfunctional organelles and damaged macromolecules during aging process. Appropriate induction or accurate regulation of autophagic process and improved quality control of mitochondria through autophagy or other strategies are required for the maintenance of skeletal muscle mass. In this article, we have summarized the current understanding of autophagic pathways in sarcopenia, and discussed the functional status of autophagy and autophagy-associated quality control of mitochondria in the pathogenesis of sarcopenia. Moreover, this article will provide some theoretical references for the exploration of scientific and optimal intervention strategies such as exercise and caloric restriction for the prevention and treatment of sarcopenia through the regulation of autophagic pathways.

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Single bout of running exercise changes LC3-II expression in rat cardiac muscle

Cited by 57 publications

References 28 publications

Cardiac Kinetophagy Coincides with Activation of Anabolic Signaling

Cardiac Kinetophagy Coincides with Activation of Anabolic Signaling

Autophagy and cell growth – the yin and yang of nutrient responses

Autophagy as a Potential Target for Sarcopenia

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