Science Note
[Aug. 20, 2024] Previous Science Note
Autophagy for Cellular Homeostasis
Cell death and the dysfunction of autophagy and lysosomes are closely linked in maintaining cellular health. When autophagy is impaired, cells cannot effectively degrade and recycle damaged components, leading to the accumulation of toxic materials and cellular stress. Lysosomal dysfunction exacerbates this problem, as these organelles are essential for the degradation of autophagosomal contents. The resulting cellular damage and stress can trigger cell death pathways that contribute to various diseases, including neurodegenerative disorders and cancer. |
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Tumor suppressor Par-4 activates autophagy-dependent ferroptosis Click here for the original article: Karthikeyan Subburayan, et. al., Communications Biology, 2024. |
The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34 Click here for the original article: Rasmus Berglund, et. al., Nature Communications, 2024. |
Autophagy counters inflammation-driven glycolytic impairment in aging hematopoietic stem cells Click here for the original article: Paul Dellorusso, et. al., Cell Stem Cell, 2024. |
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Point of Interest - Upregulation of Par-4 promotes NCOA4-dependent ferritinophagy, a selective autophagy process that degrades ferritin, increasing free iron release, lipid peroxidation, and ROS production. - Par-4 inhibition blocks ferroptosis-driven tumor suppression, highlighting its potential for cancer therapy. |
Point of Interest - This population is found to be dependent on IL-34, a ligand for CSF1R. - Loss of autophagy-dependent microglia leads to neuronal and glial cell death and increased mortality in aged mice exposed to neuroinflammation. - Conversely, IL-34-mediated microglial expansion is protective. |
Point of Interest - Inflammation suppresses glucose uptake and suppresses glycolysis in oHSCs via Socs3 inhibition of AKT/FoxO signaling, but Socs3-mediated autophagy allows metabolic compensation and a shift toward adaptive lipid metabolism. - Fasting/refeeding restores the glycolytic state and enhances the regenerative potential of oHSCs. |
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Related Techniques | ||||
First-time autophagy research | Autophagic Flux Assay Kit | |||
Autophagy detection | DAPRed (Autophagosome detection), DALGreen (Autolysosome detection) | |||
Ferrous ion (Fe2+) detection | FerroOrange(intracellular), Mito-FerroGreen(mitochondrial) | |||
Glutathione Quantification | GSSG/GSH Quantification Kit | |||
Lysosomal function | Lysosomal Acidic pH Detection Kit-Green/Red and Green/Deep Red | |||
Total ROS detection | Highly sensitive DCFH-DA or Photo-oxidation Resistant DCFH-DA | |||
Cellular senescence detection | SPiDER-βGal for live-cell imaging or flow cytometry / microplate reader / tissue samples. | |||
Glycolysis/Oxidative phosphorylation Assay | Extracellular OCR Plate Assay Kit, Glycolysis/OXPHOS Assay Kit | |||
Glucose Uptake Capacity Assay | Glucose Uptake Assay Kit-Blue/ Green/ Red | |||
Related Applications | ||||
Analysis of autophagic flux without transfection
Experimental Data
Experimental Conditions Procedure Products in Use
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