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| http://dx.doi.org/10.1002/mco2.231 | DOI Listing |
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Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis.
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School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Mitochondrial homeostasis is crucial for maintaining cellular energy production and preventing oxidative stress, which is essential for overall cellular function and longevity. Mitochondrial damage and dysfunction often occur concomitantly in myocardial ischemia-reperfusion injury (MIRI). Notoginsenoside R1 (NGR1), a unique saponin from the traditional Chinese medicine Panax notoginseng, has been shown to alleviate MIRI in previous studies, though its precise mechanism remains unclear.
View Article and Find Full Text PDFOptineurin Cooperates With NRF2 to Regulate Tooth Root Morphogenesis by Controlling Mitochondrial Dynamics and Apoptosis.
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Department of Orthodontics, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Tooth root development is a complex process essential for tooth function, yet the role of root dentin development in tooth morphogenesis is not fully understood. Optineurin (OPTN), linked to bone disorders like Paget's disease of bone (PDB), may affect tooth root development. In this study, we used single-cell sequencing of embryonic day 16.
View Article and Find Full Text PDFCopper doped bioactive glass promotes matrix vesicles-mediated biomineralization via osteoblast mitophagy and mitochondrial dynamics during bone regeneration.
Bioact Mater
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Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, 210029, Nanjing, China.
Article Synopsis
- Bone defect repair is a significant challenge in orthopedics, with copper being essential for bone regeneration, but its exact role and mechanisms in this process require further investigation.
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Mitochondrial pathways of copper neurotoxicity: focus on mitochondrial dynamics and mitophagy.
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Copper (Cu) is essential for brain development and function, yet its overload induces neuronal damage and contributes to neurodegeneration and other neurological disorders. Multiple studies demonstrated that Cu neurotoxicity is associated with mitochondrial dysfunction, routinely assessed by reduction of mitochondrial membrane potential. Nonetheless, the role of alterations of mitochondrial dynamics in brain mitochondrial dysfunction induced by Cu exposure is still debatable.
View Article and Find Full Text PDFMitochondrial fission is required for thermogenesis in brown adipose tissue.
PLoS One
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Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Maidashi, Higashi-ku, Fukuoka, Japan.
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