Ke Liu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Ke Liu has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- Shiyu Lin
Hunan key laboratory of the research and development of novel pharmaceutical preparations, Changsha Medical University, Changsha 410219, China
2 shared publications - An Li
Key Laboratory of Molecular Epidemiology of Hunan Province, Health Science Center, Hunan Normal University, Changsha, China
1 shared publication - Bin Lan
Hunan key laboratory of the research and development of novel pharmaceutical preparations, Changsha Medical University, Changsha 410219, China
1 shared publication - Fenqi Lin
Hunan key laboratory of the research and development of novel pharmaceutical preparations, Changsha Medical University, Changsha 410219, China
1 shared publication - Hanwen Zheng
Hunan key laboratory of the research and development of novel pharmaceutical preparations, Changsha Medical University, Changsha 410219, China
1 shared publication - Hui Zhen
Hunan Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, School of Public Health, Changsha Medical University, Changsha, China
1 shared publication
Latest Publications
- Open Access
- 10 November 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (11) , 1459
Adipose–Liver–Brain Redox Crosstalk in Obesity-Associated Cognitive Vulnerability: A Narrative Review
Background: Obesity-associated cognitive vulnerability involves peripheral metabolic organs, the circulation, and the neurovascular unit/blood–brain barrier (NVU/BBB). Whether adipose and hepatic dysfunction contribute through compartment-specific redox remodelling remains unclear. Methods: We searched PubMed/MEDLINE, Web of Science Core Collection, and Scopus for human, rodent, and cellular studies published from 1 January 2017 to 13 September 2026. Ninety-seven publications met the inclusion criteria. No meta-analysis or formal risk-of-bias assessment was undertaken. Results: Human studies associated adipose or hepatic dysfunction and circulating redox markers with brain and cognitive outcomes but rarely established tissue origin, temporal ordering, or mediation. Animal and cellular studies supported adipose mitochondrial and NOX-derived ROS, MASLD/MASH-related hepatic redox dysfunction, liver-derived signals, NVU/BBB impairment, and brain mitochondrial, inflammatory, synaptic, and cognitive changes. Conclusions: The adipose–liver–brain network is biologically plausible but remains unproven as a causal model. Future longitudinal and intervention studies should establish compartment specificity, temporal ordering, mediator reproducibility, reversibility, and domain-specific cognitive effects.
- 10 November 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (11) , 1459
Open AccessAdipose–Liver–Brain Redox Crosstalk in Obesity-Associated Cognitive Vulnerability: A Narrative Review
Background: Obesity-associated cognitive vulnerability involves peripheral metabolic organs, the circulation, and the neurovascular unit/blood–brain barrier (NVU/BBB). Whether adipose and hepatic dysfunction contribute through compartment-specific redox remodelling remains unclear. Methods: We searched PubMed/MEDLINE, Web of Science Core Collection, and Scopus for human, rodent, and cellular studies published from 1 January 2017 to 13 September 2026. Ninety-seven publications met the inclusion criteria. No meta-analysis or formal risk-of-bias assessment was undertaken. Results: Human studies associated adipose or hepatic dysfunction and circulating redox markers with brain and cognitive outcomes but rarely established tissue origin, temporal ordering, or mediation. Animal and cellular studies supported adipose mitochondrial and NOX-derived ROS, MASLD/MASH-related hepatic redox dysfunction, liver-derived signals, NVU/BBB impairment, and brain mitochondrial, inflammatory, synaptic, and cognitive changes. Conclusions: The adipose–liver–brain network is biologically plausible but remains unproven as a causal model. Future longitudinal and intervention studies should establish compartment specificity, temporal ordering, mediator reproducibility, reversibility, and domain-specific cognitive effects.