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PA overload elicits a maladaptive stress response characterized by endoplasmic reticulum (ER) stress, disrupted intracellular calcium homeostasis, and impaired autophagic flux, ultimately promoting cell death. Although omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA) protect against PA-induced lipotoxicity (PA-LTx), the mechanisms linking lipid handling, ER stress, and autophagy in Schwann cells remain poorly defined. Here, we investigated how PA and DHA regulate autophagic flux, ER stress signaling, and fatty acid\u2013binding protein 5 (FABP5)\u2013dependent lipid trafficking in immortalized Schwann cells (ISCs). PA exposure (300 \u00b5M PA:150 \u00b5M BSA, 24\u201348\u00a0h) significantly reduced cell viability, impaired autophagic flux as indicated by LC3-II and p62 accumulation, disrupted autophagosome\u2013autolysosome balance, and increased susceptibility to autophagic inhibition by chloroquine. DHA co-treatment (50 \u00b5M) preserved cell viability, restored autophagic flux, and normalized autophagosome\u2013autolysosome fusion. Mechanistically, PA induced ER stress marked by increased CHOP, ATF4, and Xbp1 expression, along with progressive ER calcium depletion, whereas DHA suppressed these responses and stabilized calcium homeostasis. Building on prior evidence that FABP5 protects neuron-like cells from PA-LTx, we identified a regulatory role for FABP5 in Schwann cells. PA robustly induced FABP5 expression, which was normalized by DHA and modulated by pharmacological manipulation of autophagy. FABP5 silencing exacerbated PA-induced ER stress, triggered a dysfunctional compensatory autophagy response, and impaired DHA-induced lipid droplet formation. Collectively, these findings demonstrate that functional autophagy and FABP5-dependent lipid buffering are critical adaptive responses to lipotoxic stress in Schwann cells, highlighting these pathways as potential therapeutic targets for NP-associated metabolic neuropathies.<\/jats:p>","DOI":"10.1007\/s11064-026-04841-4","type":"journal-article","created":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T06:27:49Z","timestamp":1784960869000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Docosahexaenoic Acid Protects Schwann Cells Against Palmitic Acid\u2013Induced Lipotoxicity by Modulating Autophagy, ER Stress, and Lipid Handling"],"prefix":"10.1007","volume":"51","author":[{"given":"Francis","family":"Zamora","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo-Wen","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Viet Hoang","family":"Dinh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alfonso M.","family":"Duran","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marino A.","family":"De Le\u00f3n","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4769-8736","authenticated-orcid":false,"given":"Johnny D.","family":"Figueroa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,25]]},"reference":[{"issue":"3","key":"4841_CR1","doi-asserted-by":"publisher","first-page":"265","DOI":"10.1503\/cmaj.060146","volume":"175","author":"I Gilron","year":"2006","unstructured":"Gilron I, Watson CP, Cahill CM, Moulin DE (2006) Neuropathic pain: a practical guide for the clinician. 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