Why cancer? The mechanisms that drive and maintain tumorigenesis are still a mystery. This is a play with different actors who have different roles in several contexts. One of these scenarios is represented by genetic and epigenetic conditions that determine the early trajectories of cancer cells. In addition, different mechanisms will control phenotypes and states that can take one or another direction toward cancer.
Treatment of osteoarthritis (OA) is still a challenge, since it is focused on symptom relief but fails at dealing with the progressive cartilage deterioration that occurs during the disease. Researchers from Innovo Therapeutics Inc. recently unveiled INV-1498, a caspase inhibitor, as a preclinical candidate for the treatment of OA.
Based on previous studies that have demonstrated the potential of growth hormone-releasing hormone receptor (GHRH-R) antagonists to modulate immune responses to bleomycin lung injury, researchers from the University of Miami and affiliated organizations aimed to evaluate the potential of the GHRH-R antagonist MIA-602 in a mouse model of rVSV-SARS-CoV-2-induced pulmonary dysfunction and heart injury.
Inhibition of receptor-interacting serine/threonine-protein kinase 2 (RIPK2) has been previously described as a promising strategy for the treatment of inflammatory bowel disease, as RIPK2 is a key player in the signaling leading to bacterial peptidoglycan (PGN)-induced inflammation and it amplifies pro-inflammatory responses in the intestine.
Researchers from Lerna Biopharma Pte. Ltd. (formerly Cargene Therapeutics Pte. Ltd.) recently presented the discovery and preclinical evaluation of a first-in-class GalNAc-siRNA therapeutic, CG-LR1, being developed for the treatment of liver diseases.
CVI Pharmaceuticals has presented preclinical data on their thyroid hormone receptor beta (THRB) selective agonist CVI-2742 for the potential treatment of NASH. Selective activation of the THRB contributes to ameliorating the symptoms of nonalcoholic steatohepatitis (NASH), such as liver inflammation and fibrosis, hepatocyte ballooning and liver steatosis.
REV-ERBα (NR1D1) is a circadian transcriptional repressor that plays a role in the regulation of lipid metabolism and macrophage function, and the global deletion of REV-ERBα has been previously linked to increased microglial activation and mitigation of amyloid plaque formation. In the current study, researchers from Washington University in St Louis and affiliated organizations aimed to explore the cell-autonomous effects of microglial REV-ERBα on tau pathology.
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