Yinqin Hu

Introduction With improvements in living standards, metabolic disorders have increasingly become a global public health concern. Carotid plaque and fatty liver disease, which are important target organ damages, continue to rise in prevalence. Carotid plaque is a major risk factor for cardiovascular disease (CVD), with a prevalence rate as high as 40% in people aged 40 and above (1).

Abstract Cardiac fibrosis, characterized by excessive extracellular matrix deposition, is a critical contributor to cardiovascular diseases, including heart failure. Transforming growth factor-beta 1 signaling, especially through activin receptor-like kinase 5 (ALK5), plays a key role in cardiac fibroblast activation and fibrosis. Traditional drug discovery approaches face challenges in identifying ALK5 inhibitors.

Background: Heart failure (HF) has been reported to affect cerebral cortex structure, but the underlying cause has not been determined. This study used Mendelian randomization (MR) to reveal the causal relationship between HF and structural changes in the cerebral cortex. Methods: HF was defined as the exposure variable, and cerebral cortex structure was defined as the outcome variable.