中南大学学报(医学版)最新文献

The metabolism of lipids such as fatty acids, cholesterol, and phospholipids in the brain plays a critical role in maintaining neuronal membrane structure, signal transduction, and neurotransmitter regulation. In recent years, studies have found a close association between dysregulated lipid metabolism and the development of depression. Disruption of lipid metabolism may affect the function of neural networks, leading to impaired emotional regulation and an increased risk of depression. Therefore, an in-depth exploration of the relationship between lipids and depression is of great significance for elucidating the biological basis and pathogenesis of depression. This review systematically summarizes dysregulation of 3 categories of lipid metabolism, fatty acids, cholesterol, and phospholipids, and their potential mechanisms in influencing the onset of depression through pathways such as regulation of neurotransmitters, mediation of inflammatory responses, and involvement in oxidative stress pathways. It also summarizes 4 categories of existing antidepressant treatment strategies related to brain lipid metabolism, chemical drugs, dietary interventions, traditional Chinese medicine compound formulas, and natural drugs, with the aim of clarifying the potential application value of brain lipid metabolism in the prevention and treatment of depression and providing a scientific basis for future translational directions and clinical practice in this field.

The hyaluronic acid synthase (HAS) family participates in key physiological processes such as follicular development, oocyte maturation, ovulation, and embryo implantation by regulating the synthesis of hyaluronic acid, and plays an important role in the female reproductive system. In recent years, studies have found that the HAS family exerts important regulatory effects in female infertility-related diseases. HAS2 plays a critical role in cumulus expansion and oocyte maturation, and abnormal expression of HAS2 may lead to impaired cumulus expansion and ovulatory disorders. HAS1 and HAS3 are associated with ovarian dysfunction and decreased endometrial receptivity. In addition, abnormal expression of the HAS family is closely related to infertility-related diseases such as polycystic ovary syndrome, endometriosis, and premature ovarian insufficiency. Systematic elucidation of the roles of the HAS family will not only help to deepen the understanding of the pathological mechanisms of female infertility-related diseases, but is also expected to provide key theoretical evidence and precise interventional targets for the development of novel diagnostic biomarkers, optimization of ovulation induction protocols, and improvement of embryo implantation success rates, ultimately promoting the individualized diagnosis and treatment of female infertility.

Intimal hyperplasia and pseudoaneurysm formation after vascular graft implantation are key factors affecting long-term graft patency. The transforming growth factor-beta 1 (TGF-β1) signaling pathway, through Smad-dependent and non-Smad pathways, differentially regulates smooth muscle cell phenotypic switching and proliferation, shapes the immune-inflammatory microenvironment, influences the quality of the re-endothelialization process, and maintains the balance between extracellular matrix synthesis and degradation, thereby playing a central role in the occurrence and progression of graft stenosis and pseudoaneurysm. A spatiotemporal regulatory strategy that locally inhibits excessive activation of this pathway during the inflammatory and proliferative phases, while moderately enhancing its signaling during the remodeling and maturation phase to promote matrix homeostasis, may provide new ideas for the simultaneous prevention and treatment of restenosis and pseudoaneurysm. At present, intervention approaches such as local sustained-release systems, functional modification of tissue-engineered vessels, and gene and nucleic acid therapeutics are gradually being translated into clinical practice, aiming to achieve precise spatiotemporal regulation of TGF-β1 signaling. Future studies need to further integrate single-cell and spatial multi-omics technologies to elucidate patient heterogeneity in TGF-β1 signaling and to focus on developing intelligent, responsive biomaterials capable of sensing and dynamically intervening in the activity of this pathway, ultimately realizing individualized, time-sequenced therapy and promoting a shift in vascular grafts management from anatomical repair toward an integrated model of functional and structural restoration.

Aiolos is a member of the Ikaros zinc-finger protein family and is encoded by the Ikaros family zinc finger 3 (IKZF3) gene. Aiolos not only plays a crucial role in controlling the normal differentiation and proliferation of lymphocytes, but studies have also found that it exhibits abnormally high expression in the early stages of the onset and development of multiple tumors. It influences the biological behavior of tumor cells not only by regulating tumor invasion and metastasis through mediating signaling pathways such as 66-kilodalton Src homology 2 domain-containing transforming protein (p66Shc), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/Twist, cellular myelocytomatosis oncogene, interferon regulatory factor 4, B-cell receptor, and nuclear factor kappa B, but also the instability of its gene affects tumor therapy, drug resistance, and patient prognosis. This suggests that IKZF3 is a good biological indicator for tumors and may become a new therapeutic target for tumors. A systematic elaboration of the latest research progress on the IKZF3 gene structure, physiological functions, tumor regulation, and treatment resistance can provide reference and scientific basis for future tumor therapy.

Glomerulopathy with fibronectin deposits (GFND) is a rare familial aggregation of autosomal dominant nephropathy. Proteinuria, hematuria, hypertension and progressive deterioration of renal function are the main clinical manifestations, which eventually develop into end-stage renal disease (ESRD). This report presents the clinical data and treatment process of a family with GFND caused by a fibronectin 1 (FN1) gene mutation. The proband was 12-year-old female patient diagnosed with GFND, who was admitted to the Department of Pediatric Nephrology, First People's Hospital of Yunnan Province, in November 2019 following the detection of proteinuria during a routine urinalysis. Genetic testing revealed the presence of the FN1 gene:c.2918A>G (p.Tyr973Cys)mutation in the patient, her father, and her sister, while no mutation was identified in her mother, consistent with previous reports. Summarized the literature reported of perfected the FN1 gene testing for GFND and analyzed the relationship between the gene and the clinical manifestations and prognosis of the disease. The reports showed that clinical heterogeneity even among family members with the same mutation. Additionally, GFND can recur after kidney transplantation. The link between gene mutations and clinical outcomes remains unclear and needs further study.