Xianlin Han

This study identifies age-associated repression of HNF4α as a driver of liver metabolic dysfunction and shows that restoring HNF4α can reverse some age-related liver defects.

This study investigates the effects of PLCγ2 deficiency in mice, showing impaired immune tolerance, myelin homeostasis disruption, and enhanced oxidative metabolism in the brain.

This study shows SARS-CoV-2 ORF3a disrupts lysosomal cholesterol export by interfering with VPS39-regulated NPC2 trafficking and BMP metabolism.

This study identifies lipid senolytics that kill senescent cells via ferroptosis, extending healthspan in mice by targeting ACSL4, LPCAT3, and ALOX15.

This study identifies a non-enzymatic role of ABHD6 in regulating selective hepatic insulin resistance and MASLD through interaction with the Akt-FoxO1 axis.

This study uses single-nucleus RNA-sequencing to compare transcriptional changes in male and female mouse skeletal muscle during exercise and TFEB overexpression, revealing sex-specific metabolic adaptation mechanisms.

The paper shows ketogenesis supports PUFA homeostasis in hepatocytes by enabling FA elongation, and its disruption leads to lipid imbalances similar to MASLD.

This study identifies microglia-dependent and independent mechanisms of lipid dysregulation in Alzheimer's disease using mouse models and lipidomics.

This study investigates the relationship between sulfatide deficiency, neuroinflammation, and lipid dyshomeostasis in a mouse model, showing Trem2's role in microglia-mediated neuroinflammation but not astrogliosis or myelin lipid disruption.

This study identifies TMEM106B's role in regulating myelin lipid metabolism by interacting with galactosylceramidase in TMEM106B-deficient mice.

This study investigates the effects of PLCγ2 deficiency in mouse brains using multi-omics approaches, revealing sex-specific changes in lipid and gene expression that may link to Alzheimer's disease and aging.

This study shows that Ch25h/25HC promotes neuroinflammation and neurodegeneration in a tauopathy mouse model by enhancing proinflammatory signaling and impairing sterol synthesis.

This study shows that deleting cGAS in microglia reduces amyloid-β plaque formation and cognitive impairment in Alzheimer's disease models.

This study shows that CNS sulfatide deficiency causes sex-dependent metabolic changes in aging, with females showing more severe metabolic disruption than males.

This study identifies 667 genetic loci associated with lipid species and links 186 of them to coronary artery disease through integrative lipidomics and genomics.

This study identifies de novo lipogenesis as a critical source of fatty acids for autophagosome membrane dynamics in adipocytes, showing that Fasn deficiency impairs autophagy and p62 degradation.

The paper shows that ACLY depletion in obese mice paradoxically increases de novo lipogenesis despite reducing AcCoA levels, linked to increased SREBP1c expression.

The paper links indoxyl sulfate, a gut microbiome-derived metabolite, to anxiety symptoms and specific brain connectivity patterns in patients with depression.

The paper uses targeted metabolomics to analyze changes in acylcarnitines, amines, and lipids in response to citalopram/escitalopram treatment in MDD patients, identifying metabolic correlates of treatment response.

The paper identifies serum metabolites associated with brain amyloid-beta deposition, cognitive dysfunction, and progression to Alzheimer's disease.

This study identifies RIP-Cre25Mgn neurons expressing leptin receptors as critical for leptin's anti-dyslipidemia and glucose-lowering effects in insulin-deficient mice.

This study shows APOE2 is linked to longer lifespan regardless of Alzheimer's disease, with preserved activity and lipid metabolism playing a role.

The paper investigates sex and APOE ε4 genotype effects on metabolic alterations in Alzheimer’s disease using stratified analysis of serum metabolites.

This study identifies metabolites and pathways in serum and brain tissue associated with cognitive impairment and develops models to predict antecedent cognitive decline in older adults.

The paper identifies altered bile acid profiles in Alzheimer's disease, linking them to cognitive impairment and genetic variants through a large study.

The paper identifies associations between serum bile acid metabolites and AD biomarkers in the A/T/N framework, suggesting a potential role for bile acid pathways in AD pathophysiology.