Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects

Mejías-Peña, Yubisay; Estébanez, Brisamar; Rodriguez‐Miguelez, Paula; Fernandez‐Gonzalo, Rodrigo; Almar, Mar; Paz, José Antonio de; González‐Gallego, Javier; Cuevas, María J.

doi:10.18632/aging.101167

Cited by 78 publications

(69 citation statements)

References 49 publications

(75 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Physical exercise has also been shown to affect autophagy. Resistance exercise enhances autophagy flux in peripheral blood mononuclear cells of aged subjects [37], and acute exercise increases some autophagy markers in the cerebral cortex of mice [38]. However, a direct correlation between physical exercise-stimulated autophagy flux in the brain and the prevention of age-associated cognitive deficits is still missing.…”

Section: Autophagy In the Central Nervous System (Cns)mentioning

confidence: 99%

Autophagy and Microglia: Novel Partners in Neurodegeneration and Aging

Plaza-Zabala

Sierra-Torre

Sierra

2017

IJMS

260

210

View full text Add to dashboard Cite

Abstract:Autophagy is emerging as a core regulator of Central Nervous System (CNS) aging and neurodegeneration. In the brain, it has mostly been studied in neurons, where the delivery of toxic molecules and organelles to the lysosome by autophagy is crucial for neuronal health and survival. However, we propose that the (dys)regulation of autophagy in microglia also affects innate immune functions such as phagocytosis and inflammation, which in turn contribute to the pathophysiology of aging and neurodegenerative diseases. Herein, we first describe the basic concepts of autophagy and its regulation, discuss key aspects for its accurate monitoring at the experimental level, and summarize the evidence linking autophagy impairment to CNS senescence and disease. We focus on acute, chronic, and autoimmunity-mediated neurodegeneration, including ischemia/stroke, Alzheimer's, Parkinson's, and Huntington's diseases, and multiple sclerosis. Next, we describe the actual and potential impact of autophagy on microglial phagocytic and inflammatory function. Thus, we provide evidence of how autophagy may affect microglial phagocytosis of apoptotic cells, amyloid-β, synaptic material, and myelin debris, and regulate the progression of age-associated neurodegenerative diseases. We also discuss data linking autophagy to the regulation of the microglial inflammatory phenotype, which is known to contribute to age-related brain dysfunction. Overall, we update the current knowledge of autophagy and microglia, and highlight as yet unexplored mechanisms whereby autophagy in microglia may contribute to CNS disease and senescence.

show abstract

Section: Autophagy In the Central Nervous System (Cns)mentioning

confidence: 99%

Autophagy and Microglia: Novel Partners in Neurodegeneration and Aging

Plaza-Zabala

Sierra-Torre

Sierra

2017

IJMS

260

210

View full text Add to dashboard Cite

show abstract

“…Previous studies have reported ER stress can be trigger by obesity or metabolic factors such as lipids, glucose and cytokines [32][33][34] . was common in high-fat feeding, genetic obesity and elderly [34,35] . These results demonstrated that autophagic imbalance and ER dysfunction were the main pathway that response to the pathological factor, including lipotoxicity, inflammation and insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

In vitro treatment of 3T3-L1 adipocytes with recombinant Calcium/calmodulin-dependent Protein Kinase IV (CaMKIV) limits ER stress and improves insulin sensitivity through inhibition of autophagy via the mTOR/CREB signaling pathway

Liu

Yang

Meng

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: CaMKIV has been identified as a potential regulator of skeletal muscle glucose metabolism and insulin gene expression in the pancreas. However, the mechanism of CaMKIV involved in adipose insulin resistance is not fully understood. Autophagy has to be shown as a potential therapeutic target for ER (endoplasmic reticulum) stress and insulin resistance. The purpose of this study is to investigate the effects of CaMKIV on the ER stress, autophagic function and insulin signaling in tunicamycin treated adipocytes. Methods: In this study, we treated mature 3T3-L1 adipocytes with tunicamycin to induce ER stress. Then recombinant CaMKIV and/or targeted-siRNA of CREB and mTOR were transfected into tunicamycin treated 3T3-L1 adipocytes. The ER stress markers, autophagy activation, mTOR/CREB signaling and insulin sensitivity were analyzed by western blotting or electron microscopy. Results: CaMKIV not only reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II, as well as the reduction of p62 expression, but also improved expression of p-Akt and p-IRS-1. Moreover, CaMKIV inhibited activated ER stress and elevated insulin sensitivity inAtg7 siRNA transfected adipocytes. However, the protective effects of CaMKIV were nullified by suppression of mTOR or CREB in tunicamycin-induced adipocytes. Conclusion: This study proves recombinant CaMKIV inhibits ER stress and improves insulin signaling by regulation of autophagy. The protective effect of CaMKIV in adipocytes at least partly through mTOR/CREB signaling, which could be regarded as novel opportunities for treatment of obesity and type 2 diabetes.

show abstract

“…The resistance training for the elderly can reduce muscle decay, increase muscle strength, and improve mobility. 12 In this study, the self-developed muscle strength ladder training was used to perform resistance exercises, which helps patients to change their postures autonomously. The patient sat on a nursing bed and pulled the flexible ladder section to reciprocate the upper body to exercise the upper limbs and abdominal muscles.…”

Section: Discussionmentioning

confidence: 99%