Knowledge Tree
mitochondrial dysfunction
Facts (9)
Sources
Chronic Inflammation - StatPearls - NCBI Bookshelf ncbi.nlm.nih.gov 3 facts
claimInflammatory and biochemical inducers cause oxidative stress and mitochondrial dysfunction, including the increased production of free radical molecules, advanced glycation end products (AGEs), uric acid (urate) crystals, oxidized lipoproteins, and homocysteine.
claimIncreasing age is positively correlated with elevated levels of several inflammatory molecules, potentially due to mitochondrial dysfunction, free radical accumulation, or increased visceral body fat.
referenceBarcelos IP, Troxell RM, and Graves JS (2019) investigate the link between mitochondrial dysfunction and multiple sclerosis.
Cellular rejuvenation: molecular mechanisms and potential ... - Nature nature.com Mar 14, 2023 2 facts
claimCartilage deterioration is linked to the Senescence-Associated Secretory Phenotype (SASP), while age-related mitochondrial dysfunction and oxidative stress may cause senescence in joint tissue cells.
referencePicca et al. (2019) analyzed extracellular vesicles to gain insights into mitochondrial dysfunction and aging.
Cellular senescence: from homeostasis to pathological implications ... frontiersin.org 2 facts
referenceLin, S., Wu, B., Hu, X., Lu, H. (2024) found that Sirtuin 4 (Sirt4) downregulation contributes to chondrocyte senescence and osteoarthritis by mediating mitochondrial dysfunction, as published in the International Journal of Biological Sciences.
referencede Mello AH, Costa AB, Engel JDG, and Rezin GT authored 'Mitochondrial dysfunction in obesity'.
Mitochondria and the dynamic control of stem cell homeostasis link.springer.com Apr 16, 2018 1 fact
referenceThe research community is currently investigating several key questions regarding stem cell homeostasis: (i) Does mitochondrial impairment affect stem cell function in vivo, and can stem cells be a therapeutic target for diseases causing mitochondrial dysfunction? (ii) Is it possible to modulate cell fate identity only through metabolic-related changes, and are these mechanisms relevant in vivo? (iii) Can the relationship between energy metabolism, cellular proliferation, and mitochondrial dynamics be untangled? (iv) What is the importance of calcium balance for cell fate plasticity? (v) How can redox homeostasis be effectively targeted to enhance stem cell function and improve efficient differentiation?
Phytochemical and Pharmacological Studies of Traditionally Used ... heraldopenaccess.us 1 fact
claimSilybin induces autophagy in breast cancer via ROS-dependent mitochondrial dysfunction and loss of ATP involving BNIP3; it also prevents TPA and PMA induced MMP-9 expression and VEGF secretion via inactivation of the Raf/MEK/ERK pathway and blockade of AP-1 activation via MAPK signaling pathways, according to Wang et al. [101].