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.
Previous studies have shown that neuroinflammation within the brain significantly contributes to the development and progression of hypertension. Neurogenic hypertension is defined as chronically high blood pressure that is initiated and maintained through excessive activity of the sympathetic nervous system, and is associated with increased activation of the kinin B1 receptor (B1R). Moreover, the dysregulation of the kallikrein kinin system and its receptors, particularly B1R, is involved in cardiovascular diseases and other pathological conditions associated with inflammation.
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.
Editas Medicine Inc. has nominated a lead in vivo development candidate, EDIT-401, a potential one-time therapy designed to significantly reduce LDL cholesterol (LDL-C) levels. The in vivo gene editing medicine is designed to treat hyperlipidemia by directly editing the LDLR gene to increase LDLR protein expression and reduce LDL-C levels.
Researchers at Zhengzhou University and two of its affiliated hospitals explored in a mouse model whether brozopine might mitigate ischemia-induced vascular dementia.
Replicate Bioscience Inc. and Novo Nordisk A/S have entered into a multiyear research collaboration that will leverage Replicate’s novel self-replicating RNA (srRNA) platform to develop new therapeutic candidates to treat obesity, type 2 diabetes and other cardiometabolic diseases.
Fractalkine, when binding to its receptor CX3CR1, modulates leukocyte adhesion and acts as a chemotactic agent. The expression of cardiac CX3CR1/fractalkine is elevated in patients with heart failure and CX3CR1 antagonists may improve the cardiac function by modulation of this axis.
Haisco Pharmaceutical Group Co. Ltd. has synthesized soluble guanylate cyclase (sGC) activators reported to be useful for the treatment of cardiovascular, renal and respiratory disorders.
Cardiac hypertrophy is a main contributor to heart failure, where therapeutic options are limited. Increasing evidence exists regarding up-regulation of histone lysine-specific demethylase 4A (KDM4A) in patients with cardiac hypertrophy as a risk factor, although the mechanisms behind are not well understood.
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