Cross-talk between macrophages and tumor cells could modulate cachexia in pancreatic cancer patients. A group of scientists from the University of Oklahoma has discovered a new pathway that promoted muscle wasting after the recruitment of this immune cell in the tumor microenvironment, activating cachexia-inducing factors. Macrophage depletion and the inhibition of this signaling could be developed as a therapeutic target for this condition.
The first cellular human and mouse map focused on muscle fibers and their microenvironment has revealed both the mechanisms of deterioration of this tissue over time and its adaptive capacity for regeneration. “We intended to map the skeletal muscle, isolating all the cell types, and characterizing how they change with age,” first author Veronika Kedlian from the Wellcome Sanger Institute in Cambridge told BioWorld.
An enzyme that activates cell death could be targeted to avoid the inflammation and lung lesions caused by influenza A virus (IAV). A collaborative study demonstrated that an inhibitor of receptor-interacting serine/threonine-protein kinase 3 (RIPK3) blocked necroptosis in infected alveolar epithelial cells and prevented the consequences in the lungs of severe disease.
SARS-CoV-2 could proliferate in the lungs causing severe COVID-19 through a special type of immune cell. A group of scientists from Stanford University observed how this coronavirus infected interstitial macrophages through a CD209 receptor, triggering the inflammatory response observed in hospitalized patients.
A small molecule could provide a new therapeutic approach against organ fibrosis. Using genome-wide association (GWA) assays, a group of researchers from the Westmead Institute for Medical Research in Sydney identified Mer tyrosine kinase (MERTK) as a candidate to study fibrosis and showed that its inhibition with the experimental compound reduced this condition in mouse models’ liver, kidneys and lungs. “There were some studies on the role of MERTK in liver fibrosis, but its therapeutic potential for various organ fibrosis has not been explored before. This study provides unequivocal evidence that MERTK is a potent nodal regulator of fibrosis supported by detailed mechanistic studies,” the senior author Mohammed Eslam told BioWorld.
Deep learning algorithms have enabled the discovery of molecular structures of interest in biomedicine to design treatments against aggressive diseases such as idiopathic pulmonary fibrosis (IPF). Scientists at Insilico Medicine Inc. selected a target for IPF using artificial intelligence (AI), then designed an inhibitor to block it, and tested it in vitro, in vivo, and in clinical trials.
A metabolite that suppresses appetite and food intake after exercise could be the reason for the weight loss observed in patients treated with metformin to control blood glucose. A study conducted by a group of scientists at Stanford University showed how this antidiabetic drug induced the biosynthesis of N-lactoyl-phenylalanine (Lac-Phe), which has an effect reducing the body mass index.
Scientists at the Weizmann Institute of Science in Israel announced the discovery of the new intestinal microbiota species Kazachstania weizmannii in mice, which competed with and limited the growth of Candida albicans, thus preventing candidiasis. Both microorganisms belong to the Saccharomycetaceae family and reside in humans, maintaining a complex interaction with therapeutic value.
Mapping brain circuits and studying the neural signals that are activated during post-traumatic stress could provide an answer to the generalized fear associated with this disorder. Scientists at the University of California, San Diego have identified a change in the expression of neurotransmitters as an adaptive response that could trigger this effect.
One topic at the 31st Conference on Retroviruses and Opportunistic Infections (CROI 2024) held in Denver this month was that resistance to antiretroviral therapy (ART) has become a public health problem for people living with HIV. Without a vaccine or a cure, these patients depend on treatments that suppress viremia by preventing the virus from replicating. They are lifelong treatments and, until new advances succeed in eradicating the virus from reservoirs, the only option available.