Pro-apoptotic effect of anti-β1-adrenergic receptor antibodies in periodontitis patients

Decreased autophagy induced by β1-adrenoceptor autoantibodies contributes to cardiomyocyte apoptosis

“…It has been demonstrated that cardiomyocyte apoptosis aggravated cardiac insufficiency by participating in the remodeling of the left ventricle 17 . Studies have confirmed that β 1 -AABs led to the activation of the cAMP-dependent protein kinase signaling pathway, thereby increasing caspase-3 activity, resulting in cardiomyocyte apoptosis 18 . Therefore, cardiomyocyte apoptosis induced by β 1 -AABs is one of the major factors leading to cardiac dysfunction 19 .…”

Monoclonal anti-β1-adrenergic receptor antibodies activate G protein signaling in the absence of β-arrestin recruitment

“…It has been reported that autoantibodies mapping to the β 1 AR ECL2 are highly pathogenic in a variety of cardiomyopathy conditions, inducing aortic dysfunction and ventricular arrhythmia, 27,28 thought to be mediated by pro-apoptotic effects. 29 Additionally, β 1 AR autoantibodies have been described as potent agonists of the ERK1/2 pathway 30 and increase tumor necrosis factor secretion in RAW264.7 macrophages, which is thought to be PKA-dependent. 31 A review summarizing the role and mechanisms of cardiac autoantibodies in cardiomyopathy demonstrates that β 1 AR autoantibodies play a significant role in the pathophysiology of heart failure.…”

miR‐181b promotes cell proliferation and reduces apoptosis by repressing the expression of adenylyl cyclase 9 (AC9) in cervical cancer cells

“…Cyclic AMP (cAMP) is produced from ATP by 10 different isoforms of AC in mammals, including the membrane‐bound AC1‐AC9 isoforms and a soluble AC isoform, and can be degraded into 5′‐AMP by phosphodiesterases [12–14]. As a second messenger, cAMP can either stimulate or inhibit apoptosis [15–18]. In HeLa cells, cAMP inhibits cell growth and promotes apoptosis [19], and cAMP analogs could potentially be used as anti‐cancer drugs [20,21].…”