Novartis AG has synthesized naphthyridinone derivatives acting as K(ir) 3.1/3.4 (GIRK1/4; KCNJ3/5) IKACh channel blockers reported to be useful for the treatment of bradyrhythmic arrhythmia, bradycardia, atrial fibrillation, heart block, hypotension, primary aldosteronism, sick sinus syndrome and vasovagal syncope, among others.
Verve Therapeutics Inc. has entered into an exclusive research collaboration with Eli Lilly and Co. focused on advancing Verve’s preclinical stage in vivo gene editing program targeting lipoprotein(a) (Lp[a]), a risk factor for atherosclerotic cardiovascular disease (ASCVD), ischemic stroke, thrombosis and aortic stenosis.
In recent work, researchers from Mount Sinai School of Medicine applied a drug repurposing approach to identify candidates that could target inflammation in atherosclerosis.
Thryv Therapeutics Inc. has announced the closing of a $5 million convertible note investment, the proceeds of which will be used to accelerate development of its pipeline, including preclinical programs in anaplastic thyroid carcinoma and atrial fibrillation.
Vascular smooth muscle cell (VSMC) activation plays a crucial role in the development of several vascular diseases, including intimal hyperplasia indicative of restenosis. Fragile X-related protein 1 (FXR1) is a muscle-enhanced RNA binding protein that has been proposed to regulate inflammation negatively and is overexpressed in injured arteries. However, the role of FXR1 in vascular disease remains unclear.
Research led by the Hubrecht Institute and the University Medical Center Utrecht has uncovered a key molecular mechanism that helps control heart regeneration in zebrafish. A protein known as leucine-rich repeat-containing 10 (LRRC10) acts as a switch to stop uncontrolled proliferation of cardiomyocyte cells when regeneration is complete. As reported in the May 18, 2023, issue of Science, lead author Jeroen Bakkers and colleagues found that the LRRC10 pathway was conserved in mouse and human cells.
There is a need regarding cardiovascular disease and heart failure for a therapy that reverses the progression of ventricular dysfunction. Previous findings have shown that cardiomyocytes during cardiac dysfunction show an accelerated telomere shortening, thus leading to DNA damage.
Arrhythmogenic cardiomyopathy (ACM) is a devastating inherited disorder characterized by massive cardiomyocyte loss, fibrofatty infiltration and ventricular arrhythmias, among others. Most known genetic causes of ACM involve the gene PKP2, which encodes plakophilin-2. An unmet medical need exists regarding therapies that correct this PKP2 deficiency.
Heart disease caused by damage to blood vessels is the leading cause of death worldwide. Arteries become clogged with fats and cholesterol when certain proteins in the body, known as lipoproteins, combine with and transport fats in the blood to cells. Scientists have long believed that the LDL receptor molecule was responsible for the intracellular transport of LDL. But given that some individuals lacking the LDL receptor still have high levels of LDL, questions remain about the mechanism.
Despite advances in diagnosis and treatment, cardiovascular disease remains the leading cause of death worldwide. Single-nucleotide polymorphisms (SNPs) in microRNAs are known to play important roles in acute coronary syndrome (ACS). MicroRNA 146a (miR-146a) is significantly upregulated in human atherosclerotic plaques and its circulating levels are elevated in patients with ACS, and was thus the focus of a recent study.
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