Pulmonary arterial hypertension (PAH) is a condition that may lead to right heart dysfunction. Previous evidence has tied mitochondrial dynamics with the progression of PAH, but the mechanisms behind this are not well elucidated.
“New explosions in biotechnology are allowing us to interrogate cancers at a very sophisticated level compared to before,” Dennis Slamon told audience members at the Global Bio Conference in Seoul, South Korea Sept. 3.
Pulmonary arterial hypertension (PAH) is a life-threatening disease; vasodilators may aid in managing this condition, but their impact on prognosis is still limited, potentially due to a lack of biomarkers to guide therapy. Japanese researchers have presented results of their efforts to discover potential molecular markers that may predict response to pulmonary vasodilators.
The mechanisms behind diabetic cardiomyopathy (DCM) have been deeply studied but still not well-established within the scientific community. Mutations in cardiac junction proteins may result in heart failure and arrhythmia. ER degradation enhancing α-mannosidase like protein 2 (EDEM2) is involved in the degradation of misfolded N-glycosylated proteins, but its role in the heart is not clear and was investigated.
There have been numerous improvements in the treatment of cardiovascular disease since the European Society of Cardiology (ESC) first met in 1950, but unmet medical need remains and the science continues to advance, as delegates heard at the 75th annual meeting in Madrid, Spain, Aug. 29-Sept. 1.
The addition of photoisomerizable moieties in drugs opens the possibility of rapid and reversible light-dependent switching between an active and inactive form. Researchers from the National Institutes of Health and the University of Barcelona have developed MRS-7787, a photoswitchable adenosine A3 receptor (A3R) agonist that controls A3R through topical skin irradiation.
“The impoverished laboratory environment in which mice and rats are maintained has been very good at increasing experimental replicability,” Steven Austad told the audience at the 12th Aging Research & Drug Discovery Meeting (ARDD) in Copenhagen last week. “But at the cost of sacrificing translational relevance.”
The TCF4/β-catenin axis is a key driver of tumor growth, where β-catenin has remained resistant to therapy and is traditionally considered an undruggable protein. At the ACS Fall 2025 meeting, Parabilis Medicines Inc. divulged results of work on hyperstabilized α-helical peptides named helicons that directly bind to β-catenin and block its interaction with TCF transcription factors such as TCF4, as well as inhibit the Wnt signaling pathway.
The WEE1 tyrosine kinase is an important cell cycle regulator that inhibits cell cycle progression during the S and G2/M phases to impede the division of cells with DNA damage. Tumor cells with replicative stress are thought to rely on WEE1 for their survival.
At the 12th Aging Research & Drug Discovery (ARDD) Meeting, which is being held this week in Copenhagen, Life Biosciences Inc. announced that it is developing its partial epigenetic reprogramming technology for liver disease as well as optic neuropathies. The company’s chief scientific officer Sharon Rosenzweig-Lipson estimated that its ER-100 would enter clinical trials in early 2026, putting it on track to be the first application of partial epigenetic reprogramming to enter the clinic.
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