Juqing Deng

Juqing Deng


Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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15 September 2025 in Biology
Verified
Journal Article
Open access
PDF file
WWWu Wu
Wu Wu
JLJiaxin Liu
Jiaxin Liu
YLYanWen Li
YanWen Li
FDFang Du
Fang Du
WLWei Jia Li
Wei Jia Li
JDJuqing Deng
Juqing Deng
Ischemic stroke induces complex neuroinflammatory cascades, where microglial autophagy and mitophagy serve dual roles in both injury amplification and tissue repair. This scoping review synthesized current evidence on their regulatory mechanisms and therapeutic implications. Literature was identified via PubMed and Embase, yielding 79 records, from which 39 original research articles and 13 review papers were included after eligibility screening. Search terms included “microglia,” “autophagy,” and “ischemic stroke.” Protective autophagy was frequently associated with AMPK activation, mTOR inhibition, and mitophagy pathways such as PINK1/Parkin and BNIP3/NIX, facilitating mitochondrial clearance, M2 polarization, and anti-inflammatory signaling. Therapeutic agents such as rapamycin, Tat-Beclin 1, and Urolithin A consistently demonstrated neuroprotection in preclinical stroke models. In contrast, excessive or prolonged autophagic activation was linked to inflammasome amplification, oxidative stress, and phagoptosis. Limited human studies reported associations between elevated serum ATG5 levels or ATG7 polymorphisms and worse clinical outcomes, suggesting preliminary translational relevance. These findings support the potential of phase-specific modulation of microglial autophagy as a therapeutic avenue for stroke, although further validation in human models and development of autophagy biomarkers are needed for clinical application.

14 July 2026 in European Archives of Psychiatry and Clinical Neuroscience
Verified
Journal Article
Open access
JGJiaoqiong Guan
Jiaoqiong Guan
FWFei Wen
Fei Wen
JDJuqing Deng
Juqing Deng
KLKun Lian
Kun Lian
Depressive disorders constitute a leading global cause of disability, yet comprehensive evidence regarding their long-term trends, socioeconomic disparities, and the impact of the COVID-19 pandemic remains limited. This study aimed to investigate the global burden, epidemiological patterns, and risk factors of depressive disorders from 1990 to 2021, and to project future trends to 2050. Using Global Burden of Disease 2021 data, we analyzed spatial-temporal patterns, demographic disparities, and socioeconomic gradients with joinpoint regression, cross-lagged modeling, and SHAP analysis. We further forecasted disease burden through 2050 using time-series projection. The global burden of depressive disorders exhibited substantial geographic heterogeneity and increased continuously over the study period, with a marked acceleration after 2019. COVID-19 incidence predicts subsequent increases in depressive disorder burden at the population level. Females and individuals aged 15-49 years carried the highest disease burden, and the contribution of older adults gradually increased. Drug use, smoking, and intimate partner violence represented the leading modifiable risk factors. Burden projections indicated continuous growth through 2050 without effective public health intervention. These findings highlight persistent global inequalities in depressive disorder burden and confirm the adverse impact of COVID-19 on mental health. Targeted, cross-sectoral, and equity-oriented mental health strategies are urgently needed to alleviate the growing global burden of depressive disorders.