Liver fibrosis is a pathological process resulting from various chronic liver injuries that lead to the formation of liver fibrous scars. It can further progress to cirrhosis and even liver cancer. Currently, there are no effective drugs specifically approved for the treatment of liver fibrosis; etiological therapy remains the main treatment strategy. Therefore, it is necessary to develop anti-fibrotic drugs targeting different pathways involved in liver fibrosis. Transforming growth factor-beta (TGF-β) is a key driver of fibrosis, and targeting TGF-β can effectively reduce liver fibrosis. In this review, we discussed the anti-liver fibrosis effects of TGF-β inhibitors through different signaling pathways, including the application of certain active ingredients from Traditional Chinese Medicine.

Professor Alexander Hoffmann and Genhong Cheng from University of California, Los Angeles, jointly with Professor David Baltimore from California Institute of Technology, published a review article in the newly launched journal Immunity & Inflammation. This article provides a systematic overview of NF-κB, covering its activation mechanisms, gene regulatory networks, physiological and pathological roles. It also summarizes recent advances in therapeutic strategies targeting NF-κB, offering a critical foundation for deeper understanding the pathway’s functions and mechanisms.

The unfolded protein response (UPR) is a protective pathway that helps cells manage stress during protein production. Cancer cells exploit this system to survive harsh tumor environments. In bones, they also disrupt the balance of bone-building and bone-resorbing cells, leading to skeletal fragility. Emerging therapies that target the UPR show promise in restoring bone health while selectively killing malignant cells, offering new hope for patients with cancer-associated bone disease.

A study coordinated from Badalona by IrsiCaixa, the Catalan Institute of Oncology and the Germans Trias i Pujol Research Institute (within the CARE programme) has identified KIMA, a genomic signature that makes it possible to anticipate which patients with HR+/HER2- breast cancer will respond less well to CDK4/6 inhibitors. The finding, published in the journal Clinical and Translational Medicine, may help personalize therapies and design new combinations.

An international study led by researchers from the Department of Medicine and Life Sciences (MELIS) of Pompeu Fabra University and Stanford University (California) has designed a system to identify highly selective peptides with high therapeutic potential. The method is based on the use of biologically- and chemically-modified bacteriophages to screen, with a high degree of precision, up to 1 billion peptides simultaneously. This allows identifying those that can successfully distinguish very similar proteins that play a significant role in the development of cancer and diabetes, respectively, and that are currently being treated with non-specific drugs.