Hua Zheng

Objective: This retrospective study compared the effects of indobufen versus aspirin, each combined with clopidogrel, on serum uric acid (SUA) levels and gout attacks in patients undergoing coronary stenting. Methods: Among 213 enrolled patients, 156 were included after propensity score matching and assigned to either the indobufen plus clopidogrel group ( n = 78) or the aspirin plus clopidogrel group ( n = 78). SUA levels were measured at baseline and at the 1-month, 6-month, and 1-year follow-ups. Gout attacks and major cardiovascular events were recorded throughout the study. Results: Baseline characteristics were comparable. The indobufen group showed significant reductions in SUA levels at all follow-ups (all, P < 0.001), whereas levels in the aspirin group remained stable. Although the initial gout attack rates at baseline were similar between groups, the probability of recurrence during follow-up was lower in the indobufen group. Cardiovascular safety profiles were comparable between groups. Conclusion: Indobufen plus clopidogrel significantly reduced SUA levels and showed a favorable trend in reducing gout recurrences without compromising cardiovascular safety.

Cardiovascular disease (CVD) is one of the leading causes of death globally, characterized by high morbidity and mortality rates. Metabolic disorders are critical risk factors for CVD. In recent years, growing evidence has highlighted the crucial role of gut microbiota in the onset, progression, and pathological mechanisms of both metabolic diseases and CVD. Akkermansia muciniphila (A. muciniphila), a promising next-generation probiotic, has attracted considerable attention due to its unique metabolic functions and immunomodulatory properties. This review systematically summarizes the mechanisms and research progress regarding the role of A. muciniphila in metabolic diseases and cardiovascular diseases. It elucidates how this bacterium exerts beneficial effects on metabolic disorders through multiple pathways, including improving gut barrier function, regulating lipid and glucose metabolism, increasing short-chain fatty acid production, and suppressing inflammatory responses. Meanwhile, A. muciniphila is also involved in cardiovascular protective processes such as anti-atherosclerosis, blood pressure regulation, alleviation of atrial fibrillation, and improvement of pulmonary arterial hypertension. Its mechanisms involve immunomodulation, regulation of metabolites, and multi-level interactions along the gut-cardiovascular axis, offering novel microbial targets and strategies for intervening in related diseases.

Hypertriglyceridemia is an important contributor to atherosclerotic cardiovascular disease (ASCVD) and acute pancreatitis. Familial hypertriglyceridemia is often caused by mutations in genes involved in triglyceride metabolism. Here, we investigated the disease-causing gene mutations in a Chinese family with hypertriglyceridemia and assessed the functional significance in vitro. Whole-exome sequencing (WES) was performed revealing that the severe hypertriglyceridemic proband carried a missense mutation (c.590G > A) in exon 5 of the LPL gene, as well as a missense mutation (c.1523C > T) in exon 10 of the LMF1 gene. Conservation analysis by Polyphen-2 showed that the 508 locus in the LMF1 protein and 197 locus in the LPL protein were highly conserved between different species. I-TASSER analysis indicated that the LMF1 c.1523C > T mutation and the LPL c.590G > A mutation changed the tertiary structure of the protein. A decrease in mRNA and protein expression was observed in 293T cells transfected with plasmids carrying the LMF1 c.1523C > T mutation. Subcellular localization showed that both wild-type (WT) and mutant LMF1 protein were localized at the cell cytoplasm. In the cell medium and cell lysates, these LMF1 and LPL gene mutations both caused a decreased LPL mass. Moreover, the combination of LMF1 and LPL gene mutations significantly decreased LPL levels compared to their individual effects on the LPL concentration. Both the clinical and in vitro data suggest that severe hypertriglyceridemia was of digenic origin caused by LMF1 and LPL mutation double heterozygosity in this patient.

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Gynecologic malignancies, mainly including ovarian cancer, cervical cancer and endometrial cancer, are leading causes of death among women worldwide with high incidence and mortality rate. Recently, adoptive T cell therapy (ACT) using engineered T cells redirected by genes which encode for tumor-specific T cell receptors (TCRs) or chimeric antigen receptors (CARs) has demonstrated a delightful potency in B cell lymphoma treatment. Researches impelling ACT to be applied in treating solid tumors like gynecologic tumors are ongoing. This review summarizes the preclinical research and clinical application of engineered T cells therapy for gynecologic cancer in order to arouse new thoughts for remedies of this disease.