Myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated vasculitis is a systemic condition affecting the small vessels with production of MPO-ANCA in serum. It has been suggested that the formation of neutrophil extracellular traps (NETs) induced by MPO-ANCA is a driver of pathogenesis, with involvement of neutrophil elastase (NE), which in turn is activated by the enzyme cathepsin C.
The formation of neutrophil extracellular traps (NETs) is a common feature in the renal glomeruli of patients with antineutrophil cytoplasmic autoantibody (ANCA) vasculitis. The use of a DNA repair antibody, such as PAT-DX-1 from Patrys Ltd., could inhibit NET formation by interfering with DNA damage responses in the neutrophil, which lead to the release of DNA.
Repair Biotechnologies Inc. has reported new data showing that its lipid nanoparticle (LNP)/messenger RNA (mRNA) therapy rapidly reversed the progression of atherosclerosis in mouse models applicable to familial hypercholesterolemia as well as atherosclerosis in the broader population.
Plasma pharmacodynamic biomarkers may be a reliable tool for biosimilarity assessment without having to rely on clinical trials, which are costly and time consuming.
Artivila Biopharma has divulged azepine fused ring compounds acting as receptor-interacting serine/threonine-protein kinase 1 (RIPK1; RIP-1) inhibitors reported to be useful for the treatment of coronary heart disease, inflammatory bowel disease, liver diseases, myocardial infarction, neurodegeneration, stroke, inflammatory disorders and renal disorders, among others.
Stealth Biotherapeutics Inc. has presented new data demonstrating cardioprotective effects of SBT-589 in preclinical models of Friedreich’s ataxia (FA). SBT-589 acts on mitochondrial pathways essential for cellular health and energy production that are impaired in FA cardiomyopathy.
Previous research found that p62 is the key autophagy adapter protein and a hub of multicellular signaling involved in different physiological and pathological processes.
Researchers from the Center of Biomedical Research (Lucknow) presented data from a study that assessed the functional significance the translocation of the regulator of G protein signaling 6 (RGS6) to the nucleus in response to cytotoxic stress.
Heart failure with preserved ejection fraction (HFpEF) has limited treatment options and remains a medical challenge. HFpEF is characterized by diastolic dysfunction with a normal ejection fraction. Previous findings have shown that inhibiting histone deacetylase 6 (HDAC6) alters the mechanisms contributing to dilated cardiomyopathy.
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