Exploring molecular mechanisms of exercise on metabolic syndrome: a bibliometric and visualization study using CiteSpace.

Objective: To investigate the molecular mechanisms through which exercise influences metabolic syndrome (MS) and identify key research trends and collaborative networks using bibliometric and visualization techniques. Methods: We conducted a systematic literature search using the Web of Science Core Collection for articles published from 2014 to 2023. Using CiteSpace, we performed a bibliometric analysis of 562 eligible papers, generating visual knowledge maps to identify prevailing patterns, popular subjects, and emerging trends in the literature. Results: The study reveals that exercise mitigates MS by reversing high-fat diet-induced abdominal obesity, reducing lipid accumulation and inflammation, enhancing insulin sensitivity, and improving cardiovascular function. Key molecular pathways include PPAR-γ/CPT-1/MCAD signaling, AMPK activation, and nitric oxide production. The USA leads in research output, with significant contributions from American institutions. Collaboration among researchers is limited, highlighting the need for more extensive and high-quality research initiatives. Conclusions: Regular, moderate-to-high-intensity exercise is crucial for managing MS. Exercise activates beneficial molecular pathways, improving metabolic health and cardiovascular function. Future research should focus on expanding collaborations and exploring novel molecular targets to enhance the therapeutic potential of exercise in metabolic syndrome management.

SCD1 is the critical signaling hub to mediate metabolic diseases: Mechanism and the development of its inhibitors.

Metabolic diseases, featured with dysregulated energy homeostasis, have become major global health challenges. Patients with metabolic diseases have high probability to manifest multiple complications in lipid metabolism, e.g. obesity, insulin resistance and fatty liver. Therefore, targeting the hub genes in lipid metabolism may systemically ameliorate the metabolic diseases, along with the complications. Stearoyl-CoA desaturase 1(SCD1) is a key enzyme that desaturates the saturated fatty acids (SFAs) derived from de novo lipogenesis or diet to generate monounsaturated fatty acids (MUFAs). SCD1 maintains the metabolic and tissue homeostasis by responding to, and integrating the multiple layers of endogenous stimuli, which is mediated by the synthesized MUFAs. It critically regulates a myriad of physiological processes, including energy homeostasis, development, autophagy, tumorigenesis and inflammation. Aberrant transcriptional and epigenetic activation of SCD1 regulates AMPK/ACC, SIRT1/PGC1α, NcDase/Wnt, etc, and causes aberrant lipid accumulation, thereby promoting the progression of obesity, non-alcoholic fatty liver, diabetes and cancer. This review critically assesses the integrative mechanisms of the (patho)physiological functions of SCD1 in metabolic homeostasis, inflammation and autophagy. For translational perspective, potent SCD1 inhibitors have been developed to treat various types of cancer. We thus discuss the multidisciplinary advances that greatly accelerate the development of SCD1 new inhibitors. In conclusion, besides cancer treatment, SCD1 may serve as the promising target to combat multiple metabolic complications simultaneously.

Osteoarthritis and cardiovascular disease: A Mendelian randomization study.

Objective: This Mendelian randomization (MR) study aimed to investigate the causal relationship between osteoarthritis (OA) and cardiovascular disease (CVD). Methods: From a genome-wide association study of European ancestry, we selected single nucleotide polymorphisms for two types of OA, knee osteoarthritis (KOA) and hip osteoarthritis (HOA), as instrumental variables. We evaluated three types of CVD: coronary heart disease (CHD), heart failure (HF), and stroke. We used the traditional inverse variance weighting (IVW) method and other methods to estimate causality. Heterogeneity and sensitivity tests were also applied. Finally, we conducted a MR analysis in the opposite direction to investigate reverse causality. Results: IVW analysis showed that HOA significantly affected the incidence of HF [odds ratio (OR): 1.0675; 95% confidence interval (CI): 0.0182-0.1125, P = 0.0066]. HOA significantly affected the incidence of stroke (OR: 1.1368; 95% CI: 1.0739-1.2033, P = 9.9488e-06). CHD could dramatically affect the incidence of KOA (OR: 0.9011; 95% CI: 0.8442-0.9619, P = 0.0018). The rest of the results were negative. Conclusions: Our results revealed a potential causal relationship between HOA and risk of HF, and a potential causal relationship between HOA and risk of stroke. Our findings also suggested that CHD has a significant causal relationship with the risk of KOA. This paper may provide new ideas for the treatment of OA and CVD.