Alejandro Soto–Gutiérrez

This study identifies YY1 phosphorylation as a key mechanism linking non-apoptotic caspase-8 signaling to METRN induction and MASH fibrosis.

This study identifies KIF12 as critical for organelle localization in cholangiocytes, showing its dysfunction leads to mitochondrial, lysosomal, and cilia mislocalization in liver disease.

This study identifies hLMR1, a human-specific lncRNA, as a suppressor of hepatic amino acid catabolism and ureagenesis, linking its dysregulation to metabolic dysfunction in MAFLD.

This study successfully bioprints functional human primary and iPSC-derived islets using alginate/methylcellulose bioink, maintaining their genetic expression and metabolic functionality.

This study develops a rat model of cirrhosis-induced hepatocellular carcinoma using thioacetamide, showing fibrosis, altered liver architecture, and increased AFP levels.

This paper develops a coupled microphysiological system to study how liver dysfunction affects pancreatic islet function, finding altered secretomes and glucose responses under metabolic syndrome conditions.

This study uses a human liver microphysiology system to compare the effects of PNPLA3 variants on MASLD progression and drug response.

This study creates a human iPSC-derived hepatocyte model with the TM6SF2 E167K mutation to study its effects on lipid metabolism and MASLD.

The paper uses long-read single-cell sequencing to identify mutation-specific mRNA isoforms and fusion transcripts in liver cancer cells, improving classification of cancer versus benign cells.