Efficacy of atorvastatin calcium on clinical manifestations and serum inflammatory markers in elderly patients with hypertension.

Objective: To evaluate the effects of atorvastatin calcium on clinical manifestations and serum inflammatory markers in elderly patients with hypertension.

Methods: This retrospective cohort study included 68 elderly patients with hypertension admitted to the Chongming Branch of Shanghai Tenth People's Hospital between March 2022 and June 2023. Patients were matched into two groups, each comprising 34 participants: a control group receiving amlodipine besylate and an experimental group receiving additional atorvastatin calcium.

Elevated levels of sIL-2R, TNF-α and hs-CRP are independent risk factors for post percutaneous coronary intervention coronary slow flow in patients with non-ST segment elevation acute coronary syndrome.

To evaluate the association between circulating levels of inflammatory cytokines and the occurrence of post-percutaneous coronary intervention (PCI) coronary slow flow (CSF) in patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). CSF after PCI commonly occurs and implies poor outcomes, while the determinants of post-PCI CSF in patients with NSTE-ACS remain controversial. In this multicenter case control study, 176 patients diagnosed with NSTE-ACS and with post-PCI CSF occurred composed of CSF group, while 352 matched NSTE-ACS patients composed control group.

MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.

Endothelial-mesenchymal transition (EndMT) is a major source of transformed cardiac fibroblasts, which is reported to play a key role in cardiac fibrosis (CF), a pathogenesis of cardiovascular diseases such as heart failure, myocardial infarction and atrial fibrillation. Nonetheless, the specific mechanism underlying the progression of EndMT to CF is still largely unknown. In this study, we aimed to investigate the role of milk fat globule-EGF factor 8 (MFGE8), a kind of soluble glycoprotein, in TGF-β1-induced EndMT.

NLRC5 deficiency ameliorates cardiac fibrosis in diabetic cardiomyopathy by regulating EndMT through Smad2/3 signaling pathway.

Diabetic cardiomyopathy (DCM) is one of the main causes of heart failure in patients with diabetes. Cardiac fibrosis caused by endothelial mesenchymal transformation (EndMT) plays an important role in the pathogenesis of DCM. NLRC5 is a recently discovered immune and inflammatory regulatory molecule in the NOD-like receptor family, and is involved in organ fibrosis.

MFGE8 attenuates Ang-II-induced atrial fibrosis and vulnerability to atrial fibrillation through inhibition of TGF-β1/Smad2/3 pathway.

Atrial fibrillation (AF) is characterized by potentiated growth of atrial fibroblasts and excessive deposition of the extracellular matrix. Atrial fibrosis has emerged as a hallmark of atrial structural remodeling linked to AF. Nonetheless, the specific mechanism underlying the progression of atrial fibrosis to AF is still largely unknown.