Autophagy and metabolism

Lin, Pei Wen; Chu, Man Ling; Liu, Hsiao Sheng

doi:10.1002/kjm2.12299

Cited by 27 publications

(23 citation statements)

References 81 publications

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“…As described above, autophagy is induced by various cellular stressors [ 62 ]. Notably, autophagy can also act as a double-edged sword depending on cell and disease conditions [ 63 , 64 , 65 ].…”

Section: The Role Of Autophagy In the Health-promoting Effects Of Cordycepinmentioning

confidence: 99%

“…In contrast to podocytes, renal tubular epithelial cells (RTEC) show lower baseline levels of autophagy; however, knockout of ATG5 or ATG7 also results in tubular injury during development [ 62 ]. Similarly, inhibition of autophagy by inhibitors or gene silencing aggravates nephropathy induced by chemicals, drugs, or food components [ 70 , 71 , 72 ].…”

Section: The Role Of Autophagy In the Health-promoting Effects Of Cordycepinmentioning

confidence: 99%

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The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin

Chen

Lin

et al. 2021

Molecules

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Cordycepin is an adenosine derivative isolated from Cordyceps sinensis, which has been used as an herbal complementary and alternative medicine with various biological activities. The general anti-cancer mechanisms of cordycepin are regulated by the adenosine A3 receptor, epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (MAPKs), and glycogen synthase kinase (GSK)-3β, leading to cell cycle arrest or apoptosis. Notably, cordycepin also induces autophagy to trigger cell death, inhibits tumor metastasis, and modulates the immune system. Since the dysregulation of autophagy is associated with cancers and neuron, immune, and kidney diseases, cordycepin is considered an alternative treatment because of the involvement of cordycepin in autophagic signaling. However, the profound mechanism of autophagy induction by cordycepin has never been reviewed in detail. Therefore, in this article, we reviewed the anti-cancer and health-promoting effects of cordycepin in the neurons, kidneys, and the immune system through diverse mechanisms, including autophagy induction. We also suggest that formulation changes for cordycepin could enhance its bioactivity and bioavailability and lower its toxicity for future applications. A comprehensive understanding of the autophagy mechanism would provide novel mechanistic insight into the anti-cancer and health-promoting effects of cordycepin.

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Section: The Role Of Autophagy In the Health-promoting Effects Of Cordycepinmentioning

confidence: 99%

Section: The Role Of Autophagy In the Health-promoting Effects Of Cordycepinmentioning

confidence: 99%

The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin

Chen

Lin

et al. 2021

Molecules

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“…In this process, Beclin-1 is an essential molecule which plays a key role in the formation of autophagosomes, that can mediate the localization of other autophagic proteins to phagocytes and thus regulate the formation and maturation of autophagosomes (Menon and Dhamija, 2018;Xu and Qin, 2019;Kaur and Changotra, 2020). In an acute injury, autophagy can clear damaged organelles and convert them into energy (Tamargo-Gómez and Mariño, 2018;Yang et al, 2019;Lin et al, 2021). Therefore, moderately upregulated autophagy expression after acute injury is beneficial to tissue survival.…”

Section: Introductionmentioning

confidence: 99%

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Huang

Luo

Zhang

et al. 2021

Front. Bioeng. Biotechnol.

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Random flaps are widely used in tissue reconstruction, attributed to the lack of vascular axial limitation. Nevertheless, the distal end of the flap is prone to necrosis due to the lack of blood supply. Notoginseng triterpenes (NTs) are the active components extracted from Panax notoginseng, reducing oxygen consumption and improving the body’s tolerance to hypoxia. However, their role in random flap survival has not been elucidated. In this study, we used a mouse random skin flap model to verify that NT can promote cell proliferation and migration and that increasing blood perfusion can effectively improve the survival area of a skin flap. Our study also showed that the autophagy of random flaps after NT treatment was activated through the Beclin-1/VPS34/LC3 signaling pathway, and the therapeutic effect of NT significantly decreased after VPS34 IN inhibited autophagy. In conclusion, we have demonstrated that NT can significantly improve the survival rate of random flaps through the Beclin-1/VPS34/LC3 signaling pathway, suggesting that it might be a promising clinical treatment option.

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“…We finally investigated the metabolic alterations associated with D-idua downregulation by analyzing the expression levels of genes involved in glycolysis/glyconeogenesis and lipogenesis, as these pathways are recognized to be altered in models with defective autophagy or lysosome dysfunction [ 54 , 55 , 56 ]. In Figure 8 A, the genes used to evaluate glucose metabolism are marked in red: ATP-dependent 6-phosphofructokinase (Pfk), one of the main regulatory enzymes in glycolysis; triose phosphate isomerase (Tpi), essential for efficient ATP production; and lactate dehydrogenase (Ldh), which catalyzes the conversion of glycolysis-derived pyruvate to lactate.…”

Section: Resultsmentioning

confidence: 99%

Drosophila D-idua Reduction Mimics Mucopolysaccharidosis Type I Disease-Related Phenotypes

Filippis

Napoli

Rigon

et al. 2021

Cells

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Deficit of the IDUA (α-L-iduronidase) enzyme causes the lysosomal storage disorder mucopolysaccharidosis type I (MPS I), a rare pediatric neurometabolic disease, due to pathological variants in the IDUA gene and is characterized by the accumulation of the undegraded mucopolysaccharides heparan sulfate and dermatan sulfate into lysosomes, with secondary cellular consequences that are still mostly unclarified. Here, we report a new fruit fly RNAi-mediated knockdown model of a IDUA homolog (D-idua) displaying a phenotype mimicking some typical molecular features of Lysosomal Storage Disorders (LSD). In this study, we showed that D-idua is a vital gene in Drosophila and that ubiquitous reduction of its expression leads to lethality during the pupal stage, when the precise degradation/synthesis of macromolecules, together with a functional autophagic pathway, are indispensable for the correct development to the adult stage. Tissue-specific analysis of the D-idua model showed an increase in the number and size of lysosomes in the brain and muscle. Moreover, the incorrect acidification of lysosomes led to dysfunctional lysosome-autophagosome fusion and the consequent block of autophagy flux. A concomitant metabolic drift of glycolysis and lipogenesis pathways was observed. After starvation, D-idua larvae showed a quite complete rescue of both autophagy/lysosome phenotypes and metabolic alterations. Metabolism and autophagy are strictly interconnected vital processes that contribute to maintain homeostatic control of energy balance, and little is known about this regulation in LSDs. Our results provide new starting points for future investigations on the disease’s pathogenic mechanisms and possible pharmacological manipulations.

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Autophagy and metabolism

Cited by 27 publications

References 81 publications

The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin

The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Drosophila D-idua Reduction Mimics Mucopolysaccharidosis Type I Disease-Related Phenotypes

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