January 2022 in “Figshare” Autophagy helps mouse glands stay healthy, prevents early aging, and maintains their oil and scent production.
December 2023 in “Redox biology” The substance DMC helps get rid of aging cells by triggering a process that causes cell death, which could treat age-related diseases.
Newly designed proteins can effectively degrade specific proteins in cells, offering a potential new therapy method.
Engineered vesicles deliver mitochondria to improve diabetic wound healing.
April 2016 in “Journal of Investigative Dermatology” Autophagy, a cell recycling process, is crucial for prolonged hair growth and could be a potential target for treating hair growth disorders.
Newly designed proteins can effectively degrade specific proteins in cells, offering a promising alternative for targeted protein degradation.
1 citations
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May 2020 in “PubMed” Activating autophagy might reverse skin fibrosis.
26 citations
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December 2020 in “Nature metabolism” Rapamycin treatment helps with mitochondrial disease by reducing PKC levels.
9 citations
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December 2021 in “Journal of Cellular and Molecular Medicine” HAT-MSCs can effectively engulf harmful microbes and particles, aiding infection treatment.
60 citations
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July 2014 in “Autophagy” The protein FLCN is involved in cellular cleanup and is regulated by ULK1.
4 citations
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August 2018 in “Journal of cellular biochemistry” Acid inside cells speeds up aging and turns on aging signs in mice.
2 citations
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August 2023 in “Autophagy” Autophagy helps control skin inflammation and cancer responses and regulates hair growth by affecting stem cell activity.
November 2022 in “Journal of Investigative Dermatology” Autophagy in skin cells is important for preventing inflammation, skin tumors, and controlling hair growth timing.
344 citations
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May 2018 in “EMBO journal” Phosphorylation controls TFEB's location in the cell, affecting cell metabolism and stress response.
A molecule called α-ketobutyrate was found to extend lifespan and improve aging-related symptoms in worms and mice by activating certain cellular pathways and may help develop anti-aging treatments for humans.
December 2022 in “KSBB Journal” Activating TLR3 boosts autophagy gene expression in skin cells.
December 2020 in “Innovation in aging” Rapamycin treatment helps reduce brain inflammation and symptoms of mitochondrial disease by blocking specific pathways in mice.
3 citations
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October 2025 in “Cancer” PROTACs offer a new, precise way to treat cancer by breaking down harmful proteins.
1 citations
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July 2023 in “Nature communications” MOF controls key genes for skin development by regulating mitochondrial and ciliary functions.
2 citations
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May 2023 in “bioRxiv (Cold Spring Harbor Laboratory)” Stem cells help remove dead cells to keep tissues healthy by balancing cell replacement and clearance.
81 citations
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November 2012 in “Journal of the National Cancer Institute” The tumor suppressor gene FLCN affects mitochondrial function and energy use in cells.
5 citations
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May 2018 in “Cancer Cell” Less differentiated melanoma cells are more vulnerable to a type of cell death, which could improve cancer treatments.
44 citations
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May 2023 in “MedComm” PROTAC technology shows promise for cancer treatment but needs more effective E3 ligase recruiters.
Red light exposure slows aging in mice by improving fat metabolism.
75 citations
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February 2017 in “Aging” SkQ1 antioxidant improved health and lifespan in mice.
4 citations
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June 2024 in “The Kaohsiung Journal of Medical Sciences” Atg5 can promote tumors when autophagy is deficient but suppresses them under normal conditions.
October 2025 in “Biomolecules” Intermittent fasting improves metabolism and reduces obesity by affecting specific molecules in fat tissue.
33 citations
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September 2020 in “Current Rheumatology Reports” Targeting adipocyte-to-mesenchymal transition could help treat fibrosis.
MFN2 mutations cause mitochondrial problems, unusual fat distribution, and low leptin despite high body fat.
42 citations
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December 2016 in “Cell Death & Differentiation” Damaging mitochondrial DNA in mice speeds up aging due to increased reactive oxygen species, not through the p53/p21 pathway.