Obesity is a major global health issue and a leading contributor to cardiovascular disease (CVD). While traditional research has emphasized diet and physical inactivity, psychological factors, particularly emotional eating, are increasingly recognized as important contributors to metabolic and cardiovascular health. Emotional eating, defined as eating in response to negative emotions, represents a maladaptive coping mechanism that promotes excessive caloric intake, visceral fat accumulation, and metabolic dysregulation. Chronic stress activates the hypothalamic-pituitary-adrenal axis, leading to increased cortisol secretion and appetite, while recurrent emotional eating behaviors reinforce this biological pathway and contribute to insulin resistance, dyslipidemia, hypertension, and systemic inflammation. Together, these mechanisms link psychological stress to cardiometabolic dysfunction and ultimately to increased CVD risk. Although direct evidence linking emotional eating to clinical CVD outcomes remains limited, accumulating evidence supports its role as a behavioral mediator connecting psychological stress, metabolic abnormalities, and cardiovascular risk. Effective management of emotional eating requires an integrated approach that combines cognitive behavioral therapy, mindfulness-based strategies, stress management, healthy lifestyle modification, and pharmacological treatment for obesity when indicated. Recognizing emotional eating as a modifiable behavioral risk factor may open new opportunities for early prevention and holistic management of CVD.

Objective: Bone morphogenetic protein receptor type 2 (BMPR2) has been associated with radiographic changes in ankylosing spondylitis (AS), but further characterization of the cellular signaling pathway in osteoprogenitor (OP) is not clearly understood.The aim of this study was to investigate the expression of BMPR2 and bone morphogenetic protein 2 (BMP2)-mediated responsibility in AS. Methods: We collected 10 healthy control (HC) and 14 AS-OPs derived from facet joints. Subsequently, we then conducted RNA sequencing with two samples per group and selected BMP-related genes. Facet joint tissues and derived primary OPs were evaluated by validation of selected RNA sequencing data, immunohistochemistry, and comparison of osteogenic differentiation potential. Results: Based on RNA-sequencing analysis, we found that BMPR2 expression is higher in AS-OPs compared to in HC-OPs. We also validated the increased BMPR2 expression in facet joint tissues with AS and its derived OPs in messenger RNA and protein levels. Additionally, primary AS-OPs showed much greater response to osteogenic differentiation induced by BMP2 and a higher capacity for smad1/5/8-induced RUNX2 expression compared to HCs. Conclusion The expression of BMPR2 was found to be significantly increased in facet joint tissues of patients with AS. These findings suggest that BMPR2 may play a role in the BMP2-mediated progression of AS.