Q
Qingqing Li
Researcher at Nanjing Medical University
Publications - 20
Citations - 295
Qingqing Li is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Autophagy & Neuroprotection. The author has an hindex of 7, co-authored 18 publications receiving 188 citations.
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Journal ArticleDOI
Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1.
Yuluo Rong,Wei Liu,Chengtang Lv,Jiaxing Wang,Yongjun Luo,Dongdong Jiang,Linwei Li,Zheng Zhou,Wei Zhou,Qingqing Li,Guoyong Yin,Lipeng Yu,Jin Fan,Weihua Cai +13 more
TL;DR: The results indicate that 14-3-3t acts via a newly-discovered mechanism for the activation of autophagy by NSC-sEVs, further promoting functional behavior recovery following spinal cord injury.
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Ischemic preconditioning enhances autophagy but suppresses autophagic cell death in rat spinal neurons following ischemia-reperfusion
TL;DR: Ischemic preconditioning appears to sustain the beneficial effects of autophagic lysosomal degradation during I/R while inhibiting autophile cell death in rats subjected to ischemic spinal cord injury.
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Endogenous Parathyroid Hormone Promotes Fracture Healing by Increasing Expression of BMPR2 through cAMP/PKA/CREB Pathway in Mice.
Wei Zhou,Lipeng Yu,Jin Fan,Bowen Wan,Tao Jiang,Jian Yin,Yao Huang,Qingqing Li,Guoyong Yin,Zhaoxing Hu +9 more
TL;DR: Exogenous PTH enhanced BMPR2 expression by a cAMP/PKA/CREB pathway in osteoblasts, and increased RUNX2 expression through transduction of the BMP/pSMAD1/5/8 signaling pathway.
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Oxygen-Glucose-Deprivation/Reoxygenation-Induced Autophagic Cell Death Depends on JNK-Mediated Phosphorylation of Bcl-2.
TL;DR: The regulation of the JNK/Bcl-2/Beclin-1 signaling pathway may be one of the mechanisms underlying the OGD/R-induced autophagic cell death of neurons.
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Effect of zoledronic acid on lumbar spinal fusion in osteoporotic patients
TL;DR: Zoledronic acid accelerates spinal fusion, shortens the time of fusion without changing fusion rate, and also decreases the risk of adjacent vertebral compressing fracture and the rate of pedicle screw loosening, resulting in the improvement of clinical outcomes and quality of life.