Llanos-Becerra Graciela, Valdez-Vega Rodolfo Iván, Rosas-Carrasco Oscar, Torres-Carrillo Norma, Ibarra-Montero Priscila Iveth, Velasco-Pérez Nidia Guadalupe, Beltrán-Ramírez Raúl, Torres-Carrillo Nora Magdalena
Departamento de Microbiología y Patología Centro de Investigación en Enfermedades Infectocontagiosas, Centro Universitario de Ciencias de la Salud Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
Departamento de Salud, Universidad Iberoamericana, Ciudad de México, Mexico.
Mol Biol Rep. 2025 Sep 20;52(1):931. doi: 10.1007/s11033-025-11039-4.
Considering the key role of inflammation in sarcopenia pathogenesis, we focused on tumor necrosis factor (TNF). We examined associations between TNF promoter single-nucleotide polymorphisms (SNPs; rs1799964, rs1799724, and rs361525), individually and as haplotypes, with serum TNF-α levels and sarcopenia in older Mexican adults.
This cross-sectional study included Mexican adults aged 70 years or older. Sarcopenia was defined using calf circumference as a proxy for muscle mass, plus grip strength and physical performance, according to the European Working Group on Sarcopenia in Older People (EWGSOP) criteria. Serum TNF-α was measured by enzyme immunoassay, SNPs were genotyped using TaqMan assays, and haplotypes were estimated using haplo.stats and HAPLOVIEW. Among 223 participants, 45 had sarcopenia. rs1799964 was associated with grip strength in the total sample (OR = 0.08, 95%CI = 0.01-0.86, p = 0.014) and with calf circumference in men (OR = 0.08, 95%CI = 0.01-0.96, p = 0.014). rs1799724 was associated with poor physical performance (OR = 1.88, 95%CI = 1.04-3.37, p = 0.032), as was the TTG haplotype (OR = 1.85, 95%CI = 1.10-3.11, p = 0.019). Serum TNF-α was inversely correlated with Physical Performance (rho= -0.142, p = 0.047).
Our findings suggest that TNF promoter SNPs may be associated with specific components of sarcopenia, but not with serum TNF-α levels or the presence of sarcopenia in older Mexican adults. These results are exploratory and should be interpreted with caution, highlighting the need for further research to confirm and clarify these associations.
考虑到炎症在肌肉减少症发病机制中的关键作用，我们聚焦于肿瘤坏死因子（TNF）。我们研究了TNF启动子单核苷酸多态性（SNP；rs1799964、rs1799724和rs361525）个体及单倍型与墨西哥老年成年人血清TNF-α水平及肌肉减少症之间的关联。
这项横断面研究纳入了70岁及以上的墨西哥成年人。根据欧洲老年人肌肉减少症工作组（EWGSOP）标准，采用小腿围作为肌肉量的替代指标，加上握力和身体性能来定义肌肉减少症。通过酶免疫测定法测量血清TNF-α，使用TaqMan测定法对SNP进行基因分型，并使用haplo.stats和HAPLOVIEW估计单倍型。在223名参与者中，45人患有肌肉减少症。rs1799964与总样本中的握力相关（OR = 0.08，95%CI = 0.01 - 0.86，p = 0.014），与男性的小腿围相关（OR = 0.08，95%CI = 0.01 - 0.96，p = 0.014）。rs1799724与身体性能差相关（OR = 1.88，95%CI = 1.04 - 3.37，p = 0.032），TTG单倍型也是如此（OR = 1.85，95%CI = 1.10 - 3.11，p = 0.019）。血清TNF-α与身体性能呈负相关（rho = -0.142，p = 0.047）。
我们的研究结果表明，TNF启动子SNP可能与肌肉减少症的特定组成部分相关，但与墨西哥老年成年人的血清TNF-α水平或肌肉减少症的存在无关。这些结果具有探索性，应谨慎解释，突出了进一步研究以证实和阐明这些关联的必要性。
