Zhou et al. challenge the well-known beneficial effect of autophagy in promoting longevity. Evidence presented demonstrate that autophagy induction coupled with increased mitochondrial permeability is detrimental to organismal health in both the nematode Caenorhabditis elegans and mammals.
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| http://dx.doi.org/10.1016/j.cell.2019.03.021 | DOI Listing |
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Regulation of autophagy by protein lipidation.
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Department of Neurosurgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Autophagy is a conserved catabolic recycling pathway that can eliminate cytosolic materials to maintain homeostasis and organelle functions. Many studies over the past few decades have demonstrated that abnormal autophagy is associated with a variety of diseases. Protein lipidation plays an important role in the regulation of autophagy by affecting protein trafficking, localization, stability, interactions and signal transduction.
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Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Background: Systemic lupus erythematosus is a common autoimmune disease. Studies have suggested that defective stem cells could be involved in the pathogenesis of systemic lupus erythematosus, which leads to changes in the function of immune cells. By observing the cell morphology, autophagy, and senescence of bone marrow mesenchymal stem cells (BMSCs) from lupus mice and normal controls, this study investigated the role of IL-6 in autophagy and senescence of BMSCs and explored relevant mechanisms.
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Eye Center of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Introduction: Glaucoma, a leading cause of irreversible blindness, is characterized by optic neuropathy and retinopathy, with primary open-angle glaucoma (POAG) being the most prevalent form. The primary pathogenic mechanism of POAG involves elevated intraocular pressure caused by chronic fibrosis of the trabecular meshwork (TM). Autophagy, a critical process for maintaining cellular homeostasis, has been implicated in fibrosis across various organs.
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In age-related peripheral neurodegeneration, changes in the promotion or inhibition of endoplasmic reticulum (ER) stress response related to the ubiquitin-proteasome degradation system (UPS), autophagy and apoptosis signaling factors during aging remain unclear. In the present study, the expression of ER stress response signaling-related protein factors was examined in tibial nerves during aging in rats. Tibial nerves were extracted from continuously housed rats at 20, 50, 70, 90 and 105 weeks of age.
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Institute for Chronobiology, Foundation for Advancement of International Science (FAIS), 3-24-16 Kasuga, Tsukuba, Ibaraki, 305-0812, Japan.
Gaucher's disease (GD) is a genetic disease characterized by a mutation in the metabolic enzyme glucocerebrosidase (GBA1), leading to the accumulation of glucosylceramide in tissues. We previously discovered that a -inserted mutation in the gene of fruit flies, , mimics human neuronopathic GD (nGD) characteristics, providing a promising model for studying the molecular mechanisms of the disease. We also reported that extremely low-frequency electric fields (ELF-EFs) promote sleep and extend the lifespan of wild-type flies.
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