A common molecular pathway associated with lung fibrosis may also hold the key to pulmonary vascular repair. A group of scientists at the University of Pennsylvania (Penn) found that when a viral infection damaged these vessels, the injury could be restored by activating the transforming growth factor-β receptor 2 (TGF-βR2) in endothelial cells, which led to cell proliferation.

COVID-19 severity remains open to several questions. Researchers at the University of California Los Angeles (UCLA) have revealed how SARS-CoV-2 causes acute inflammation instead of the symptoms of a common cold. This effect could be initiated by the peptide fragments of the coronavirus released when the host eliminates the virus, which can form pro-inflammatory complexes that trigger an amplified immune response.

Bone morphogenetic protein 9 (BMP-9), also known as growth/differentiation factor 2, is a member of the transforming growth factor-β family of cytokines, which exerts its biological effects through binding to a complex formed by ALK1 and BMPR2.

Neutrophils are the immune system’s most abundant effector cells, which play a defensive role of host cells and clear pathogens by phagocytosis, degranulation and neutrophil extracellular trap (NET) release.

Be it viral, nucleic acid or protein vaccines, recent efforts that led to the first regulatory approvals for not only COVID-19, but also for malaria and respiratory syncytial virus, positioned infectious diseases in the headlines for much of the last four years.

Researchers from Scynexis Inc. have recently presented details on the preclinical characterization of SCY-247, a second-generation triterpenoid with glucan synthase inhibitor activity and intended to be used for the treatment of invasive mucormycosis.