Prostate cancer is a leading cause of cancer-related deaths among men and is a cancer type that shows genomic heterogeneity and several molecular alterations. By analyzing available microarray and next-generation transcriptome sequencing data, researchers at the University of Alabama at Birmingham found that thyroid hormone receptor-interacting protein 13 (TRIP13), a member of the AAA ATPase family, was overexpressed in prostate cancer, making it a potential therapeutic target.
Neurodegenerative disorders such as Alzheimer’s disease (AD) and frontotemporal dementia are characterized by the accumulation of hyperphosphorylated tau protein, forming neurofibrillary tangles, ultimately leading to synaptic dysfunction and cognitive decline.
Integrin alpha-5 (ITGA5) is a central modulator of extracellular matrix signaling and has been tied to fibrosis and tissue damage, contributing to lupus nephritis (LN) pathogenesis. A group of researchers aimed to investigate the association between ITGA5 and LN and its inhibition as a potential strategy to improve renal outcomes.
CD45RC is an isoform of protein tyrosine phosphatase receptor type C, a protein that plays a key role in regulating antigen receptor signaling in T and B cells. While it is expressed on most circulating B cells, it is only highly expressed on Th1 precursors, Th1 cells and T effector memory CD45RA+ cells (TEMRA).
Researchers from Beijing University of Chinese Medicine described the role of TRIM54 in cirrhosis progression using two independent animal models of chronic liver injury – a DEN-induced rat model and a CCl4-induced mouse model of liver cirrhosis.
Transforming growth factor-β-activated kinase 1 (TAK1) is a crucial central signaling molecule of hepatic cell death, inflammation and fibrogenesis through NF-κB and MAPK in metabolic dysfunction-associated steatotic liver disease (MASLD). Its pharmacological inhibition using the TAK1 inhibitor HS-276 was tested in vivo in a murine model of diet-induced MASLD.
There is a growing consensus that alcohol-related liver disease (ALD) should be considered a metabolic disorder under the influence of the gut-liver axis. Metabolome data have highlighted fatty acid-activated G protein-coupled receptors (GPCRs) as the main affected pathways, where the relationship of G-protein-coupled receptor 119 (GPR119) with ALD remains unexplored.
Adipose triglyceride lipase (ATGL), a central mediator of triglyceride hydrolysis and fatty acid mobilization, modulates hepatic lipid homeostasis and metabolic signaling pathways that contribute to the activation of fibrogenic responses.
Hepatocellular carcinoma (HCC) remains a major cause of cancer death worldwide and, although early-stage disease can sometimes be cured by surgical resection and liver transplantation, advanced cases still respond poorly to current systemic treatments and immunotherapy.
At the recently concluded European Association for the Study of the Liver meeting, presentations underscored how increasingly granular insights into liver pathobiology are driving the rapid identification of new druggable targets across diverse indications.
