Chronic low back pain (CLBP) is a common symptom of lumbar degenerative disease. Degeneration of the lumbar paravertebral muscles causes a loss of muscle mass and strength, which is a vital factor causing CLBP and often accompanied by lipid infiltration. Tandem mass spectrometry (TMT) was used to identify differentially expressed proteins in lipid-infiltrated and normal muscles. The results show that fatty acid binding protein 4 (FABP4) participated in the peroxisome proliferator-activated receptor-γ (PPAR γ) signaling pathway as an up-regulated protein, which is related to lipogenesis in diverse cells. In addition, chronic inflammation is believed to be involved in lumbar muscle degeneration and lipogenesis, with interleukin-4 (IL-4) considered as the predominant contributor. In present study, we investigate the effect of FABP4 on lipogenesis in human skeletal muscle cells (HSMCs) stimulated by Interleukin-4 (IL-4) and explore the mechanistic basis. We found expression level of FABP4 in lipid-infiltrated muscles was significantly higher than that in normal muscles. Lipogenesis in HSMCs could be increased by IL-4 treatment, as well as by FABP4 overexpression. FABP4 inhibition suppressed IL-4-mediated lipogenesis in HSMCs, whereas the PPAR γ inhibitor alleviated lipogenesis in both IL-4-treated and FABP4-overexpressed HSMCs. Collectively, the results indicate that FABP4 induces lipogenesis in HSMCs stimulated with IL-4 via activating the PPAR γ signaling pathway. Our study offers a detailed perspective on the pathogenesis of muscle lipid infiltration and provides a potential target for the clinical treatment strategy of muscle lipid infiltration and CLBP.

慢性腰痛（CLBP）是腰椎退行性疾病的常见症状。腰椎旁肌肉的退化导致肌肉质量和力量的损失，这是导致 CLBP 的重要因素，并且通常伴有脂质浸润。串联质谱 (TMT) 用于鉴定脂质浸润和正常肌肉中差异表达的蛋白质。结果表明，脂肪酸结合蛋白 4 (FABP4) 作为上调蛋白参与过氧化物酶体增殖物激活受体-γ (PPAR γ) 信号通路，这与多种细胞中的脂肪生成有关。此外，慢性炎症被认为与腰肌退化和脂肪生成有关，其中白细胞介素 4 (IL-4) 被认为是主要贡献者。在目前的研究中，我们研究了 FABP4 对白细胞介素 4 (IL-4) 刺激的人骨骼肌细胞 (HSMC) 中脂肪生成的影响，并探讨了其机制基础。我们发现脂质浸润肌肉中 FABP4 的表达水平显着高于正常肌肉中的表达水平。通过 IL-4 处理以及 FABP4 过表达，可以增加 HSMC 中的脂肪生成。FABP4 抑制抑制了 HSMC 中 IL-4 介导的脂肪生成，而 PPAR γ 抑制剂减轻了 IL-4 处理和 FABP4 过表达的 HSMC 中的脂肪生成。总的来说，结果表明 FABP4 通过激活 PPAR γ 信号通路诱导用 IL-4 刺激的 HSMC 中的脂肪生成。