Photobiomodulation at 830 nm with 5 J/cm(2) does not promote PI3K/AKT/mTOR signalling pathway activation in hyperglycemic wounded cells.

The phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) pathway regulates cell survival, proliferation, and the synthesis of protein. Photobiomodulation (PBM) stimulates biological processes by using low-powered light in the visible, red and near-infrared (NIR) spectrum. Despite its demonstrated efficacy, the cellular and molecular consequences, primarily on the PI3K/AKT/mTOR pathway, remain unclear. This study investigated PBMs impact on the PI3K/AKT/mTOR pathway in fibroblast (WS1) cells modelled as normal (N), wounded (W), hyperglycemic (D), hyperglycemic wounded (DW), and hyperglycemic hypoxic wounded (DHW). Non-irradiated cells served as controls. PBM was applied using an 830 nm diode at 5 J/cm(2). Cellular changes at 24 and 48 h post-PBM were assessed via the Trypan blue exclusion assay (viability), light microscopy (morphology and migration), flow cytometry (proliferation and apoptosis), and the enzyme linked immunosorbent assay (ELISA) and western blot (VEGF, Bcl-2, PI3K, AKT, mTOR and GSK3β). PBM enhanced cellular migration rate, viability, and proliferation, without altering the PI3K/AKT/mTOR pathway. PBM at 830 nm with 5 J/cm(2) promoted wound healing independently of the PI3K/AKT/mTOR pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10103-026-04859-8.