Publications by authors named "Sarah W Y Lok"

Article Synopsis
  • The study investigates the role of the transcription factor Foxp2 in kidney fibrosis, a key process leading to chronic kidney disease (CKD) and kidney failure, highlighting its correlation with epithelial-to-mesenchymal transition (EMT).
  • Analysis of human kidney biopsies and experiments in genetically modified mice demonstrate that increased Foxp2 expression is associated with various forms of CKD, and its deletion reduces inflammation and fibrosis in kidney tissue.
  • Findings reveal that Foxp2 influences key cellular mechanisms, including the regulation of TGF-β signaling and cell cycle, ultimately affecting the progression of kidney fibrosis through the modulation of target genes related to cell growth and ECM production.
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Synthetic data generation in omics mimics real-world biological data, providing alternatives for training and evaluation of genomic analysis tools, controlling differential expression, and exploring data architecture. We previously developed Precious1GPT, a multimodal transformer trained on transcriptomic and methylation data, along with metadata, for predicting biological age and identifying dual-purpose therapeutic targets potentially implicated in aging and age-associated diseases. In this study, we introduce Precious2GPT, a multimodal architecture that integrates Conditional Diffusion (CDiffusion) and decoder-only Multi-omics Pretrained Transformer (MoPT) models trained on gene expression and DNA methylation data.

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Article Synopsis
  • Kidney inflammation plays a significant role in worsening chronic kidney disease (CKD), and targeting TLR4 signaling might offer a new treatment approach.
  • Research showed that deleting TLR4 specifically in kidney tubules protects against kidney damage by reducing inflammation and fibrosis.
  • The study highlighted the long noncoding RNA Meg3 as a proinflammatory factor, showing that its regulation could affect cytokine production and kidney fibrosis, providing insights into TLR4's role in kidney inflammation.
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Lipotoxicity has been implicated in the pathogenesis of obesity-related kidney damage and propagates chronic kidney injury like diabetic kidney disease; however, the underlying mechanisms have not yet been fully elucidated. To date, reduction of lipid acquisition and enhancement of lipid metabolism are the major, albeit non-specific, approaches to improve lipotoxic kidney damage. In the kidneys of high-fat diet (HFD)-fed mice and tubule cells cultured with palmitic acid (PA), we observed a dramatic upregulation of the long intergenic non-coding RNA-p21 () through a p53-dependent mechanism.

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Kallistatin is a multiple functional serine protease inhibitor that protects against vascular injury, organ damage and tumor progression. Kallistatin treatment reduces inflammation and fibrosis in the progression of chronic kidney disease (CKD), but the molecular mechanisms underlying this protective process and whether kallistatin plays an endogenous role are incompletely understood. In the present study, we observed that renal kallistatin levels were significantly lower in patients with CKD.

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Background: Difference of perspective between patients and physicians over integrative medicine (IM) research and service provision remains unclear despite significant use worldwide. We observed an exceptionally low utilisation of IM and potential underreporting in diabetes. We aimed to explore the barriers and recommendations regarding service delivery and research of IM service among diabetes patients and physicians.

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Recent advances in the understanding of lipid metabolism suggest a critical role of endoplasmic reticulum (ER) stress in obesity-induced kidney injury. Hepatocyte growth factor (HGF) is a pleiotropic cytokine frequently featured in stem cell therapy with distinct renotropic benefits. This study aims to define the potential link between human induced pluripotent stem cell-derived mesenchymal stem cells (iPS-MSCs)/bone marrow-derived MSCs (BM-MSCs) and ER stress in lipotoxic kidney injury induced by palmitic acid (PA) in renal tubular cells and by high-fat diet (HFD) in mice.

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Imbalance of Wnt/β-catenin signaling in renal cells is associated with renal dysfunction, yet the precise mechanism is poorly understood. Previously we observed activated Wnt/β-catenin signaling in renal tubules during proteinuric nephropathy with an unknown net effect. Therefore, to identify the definitive role of tubular Wnt/β-catenin, we generated a novel transgenic "Tubcat" mouse conditionally expressing stabilized β-catenin specifically in renal tubules following tamoxifen administration.

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