• Fernando Guevara-Villazón, César Pacheco-Tena, Antonio Anchondo-López, Luis Alberto Ordoñez-Solorio, Benjamín Contreras Martínez, Arturo Muñoz-Cobos, Arturo Luévano-González, and Susana Aideé González-Chávez.
• Laboratorio PABIOM, Facultad de Medicina y Ciencias Biomédicas, Universidad Autónoma de Chihuahua, Circuito Universitario Campus II, 31125, Chihuahua, Chihuahua, México.
• Eur Spine J. 2023 Jun 1; 32 (6): 190119101901-1910.

PurposeTo analyze the differential transcriptome expression in hypertrophic ligaments flavum (HLF) compared to normal ligaments.MethodsA case-control study was conducted that included 15 patients with hypertrophy of LF and 15 controls. Samples of LF were obtained through a lumbar laminectomy and analyzed by DNA microarrays and histology. The dysregulated biological processes, signaling pathways, and pathological markers in the HLF were identified using bioinformatics tools.ResultsThe HLF had notable histological alterations, including hyalinosis, leukocyte infiltration, and disarrangement of collagen fibers. Transcriptomic analysis showed that up-regulated genes were associated with the signaling pathways of Rho GTPases, receptor tyrosine kinases (RTK), fibroblast growth factors (FGF), WNT, vascular endothelial growth factor, phosphoinositide 3-kinase (PIK3), mitogen-activated protein kinases, and immune system. The genes PIK3R1, RHOA, RPS27A, CDC42, VAV1, and FGF5, 9, 18, and 19 were highlighted as crucial markers in HLF. The down-expressed genes in the HLF had associations with the metabolism of RNA and proteins.ConclusionOur results suggest that abnormal processes in hypertrophied LF are mediated by the interaction of the Rho GTPase, RTK, and PI3K pathways, which have not been previously described in the HLF, but for which there are currently therapeutic proposals. More studies are required to confirm the therapeutic potential of the pathways and mediators described in our results.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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