A group of scientists from the French National Center for Scientific Research (CNRS) have overturned a scientific dogma by demonstrating, for the first time, that DNA mutations are not essential for the development of cancer. The researchers temporarily disrupted gene silencing led by Polycomb proteins in fruit flies, and observed that this could produce tumors caused only by epigenetic changes, without permanent changes to the genome.
A protein whose expression decreases during aging could be key to preserving cellular maintenance mechanisms and preventing the progressive loss of muscle mass that occurs during aging. Scientists from the Institute for Research in Biomedicine (IRB) and the University of Barcelona (UB) have revealed the role of the TP53INP2 protein in autophagy and the effects of its reduction on skeletal muscle during aging.
Scientists at Massachusetts General Hospital have linked the risk of heart failure during pregnancy and senescence proteins produced by placental aging, which could clarify how peripartum cardiomyopathy (PPCM) is triggered and opens the door to the development of cardiac function therapies in late pregnancy.
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.
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.
