A left atrial aneurysm is a very rare cardiac anomaly that usually develops in the left atrial appendage. It usually develops congenitally, and has a risk of life-threatening complications. Here, we report a case of a growing aneurysm of the left atrium that was incidentally found in a 42-yr-old woman. Eighteen years prior, an abnormal cardiomegaly was found on a chest radiography for a pre-operative study. The chest radiography at this time demonstrated a more prominent cardiomegaly than the previous radiography findings. The left atrial aneurysm was diagnosed by echocardiography and cardiac catheterization. Although asymptomatic, she underwent a successful surgical excision to allay the possibilities of rupture, arrhythmia, heart failure, or thromboembolism. The surgical findings demonstrated an 8 x 15 cm sized saccular aneurysm at the left atrial appendage, and the pathologic findings showed three myocardial layers. The patient has been asymptomatic during the 15 months of follow-up. In conclusion, a congenital left atrial aneurysm can grow with time, even in asymptomatic cases, and an aneurysmectomy is a curative treatment, which can eliminate the potential complications.
Connective tissue growth factor (CTGF) is a potent pro-fibrotic factor, which is implicated in fibrosis through extracellular matrix (ECM) induction in diabetic cardiovascular complications. It is an important downstream mediator in the fibrotic action of transforming growth factor β (TGFβ) and is potentially induced by hyperglycemia in human vascular smooth muscle cells (VSMCs). Therefore, the goal of this study is to identify the signaling pathways of CTGF effects on ECM accumulation and cell proliferation in VSMCs under hyperglycemia. We found that high glucose stimulated the levels of CTGF mRNA and protein and followed by VSMC proliferation and ECM components accumulation such as collagen type 1, collagen type 3 and fibronectin. By depleting endogenous CTGF we showed that CTGF is indispensable for the cell proliferation and ECM components accumulation in high glucose-stimulated VSMCs. In addition, pretreatment with the MEK1/2 specific inhibitors, PD98059 or U0126 potently inhibited the CTGF production and ECM components accumulation in high glucose-stimulated VSMCs. Furthermore, knockdown with ERK1/2 MAPK siRNA resulted in significantly down regulated of CTGF production, ECM components accumulation and cell proliferation in high glucose-stimulated VSMCs. Finally, ERK1/2 signaling regulated Egr-1 protein expression and treatment with recombinant CTGF reversed the Egr-1 expression in high glucose-induced VSMCs. It is conceivable that ERK1/2 MAPK signaling pathway plays an important role in regulating CTGF expression and suggests that blockade of CTGF through ERK1/2 MAPK signaling may be beneficial for therapeutic target of diabetic cardiovascular complication such as atherosclerosis.
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