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Kamzolas, I.

Publications and source records attributed to Kamzolas, I..

2 recordsLinked to original sources

Decoding MASLD Progression: A Molecular Trajectory-Based Framework for Modelling Disease Dynamics

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has emerged as a silent pandemic, affecting nearly one-third of the global population. MASLD encompasses a spectrum of liver disorders, ranging from simple steatosis to Metabolic Dysfunction-Associated Steatohepatitis (MASH), characterised by lipotoxicity, hepatocellular injury, inflammation, and fibrosis, which can eventually progress to cirrhosis and hepatocellular carcinoma. Despite the progressive nature of MASLD/MASH, current research and clinical practice primarily rely on static, histopathology-defined stages that fail to capture the continuous nature of disease progression. Here, we present an integrative framework that combines patient pseudo-temporal ordering, network analysis, and cell-type deconvolution to reconstruct the continuous MASLD/MASH trajectory. By analysing patient liver transcriptomic profiles, we position patients along this data-driven trajectory, moving beyond conventional stage-based classifications. This approach reveals the sequence of critical molecular events underlying MASLD/MASH progression, providing mechanistic insights into the diseases pathophysiology. By integrating these findings with plasma proteomics data, we identify novel trajectory-specific plasma biomarkers that predict disease stage (and trajectory position) independently of histology. Together, these findings demonstrate the value of trajectory-based frameworks for understanding MASLD pathophysiology and highlight new opportunities for precision diagnosis and therapeutic target prioritisation across the disease spectrum.

systems biology↗

Oxygen is a critical regulator of cellular metabolism and function in cell culture

Cell culture is generally considered to be hyperoxic. However, the importance of cellular oxygen consumption is often underappreciated, with rates of oxygen consumption often sufficient to cause hypoxia at cell monolayers. We initially focused on cultured adipocytes as a terminally differentiated cell-type with substantial oxygen consumption rates to support diverse cellular functions. Under standard conditions, cultured adipocytes are hypoxic and highly glycolytic. Increasing oxygen diverted glucose flux toward mitochondria and resulted in thousands of gene expression changes that pointed toward alleviated physiological transcriptional responses to hypoxia. Phenotypically, providing more oxygen increased adipokine secretion and rendered adipocytes more sensitive to insulin and lipolytic stimuli. The functional benefits of increasing pericellular oxygen were transferable to other cellular systems including hPSC-derived hepatocytes and cardiac organoids. Our findings suggest that oxygen is limiting in many terminally-differentiated cell culture systems, and that controlling oxygen availability can improve the quality and translatability of cell models.

cell biology↗