{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Yangbao Miao"],"species":["Homo Sapiens","Mus Musculus"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0016532000"],"submitter_email":["miaoyangbao@uestc.edu.cn"],"submitter_affiliation":["Sichuan Academy of Medical Sciences, Sichuan Provincial People's Hospital‌"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"Integrated proteomic profiling of human and murine tear fluid reveals ER-mitochondrial lipid crosstalk and organelle stress signaling in dry eye disease","description":"This project presents comprehensive proteomic profiling of human and murine tear fluid samples in the context of dry eye disease (DED). Human tear proteomics revealed significant activation of the PERK-ATF4 integrated stress response axis, coordinated reprogramming of mitochondrial bioenergetics (TCA cycle enzymes including IDH3A, ECHS1), and dysregulation of sterol/lipid transport pathways. Murine tear proteomics further demonstrated disruptions in endoplasmic reticulum-mitochondrial lipid exchange, including altered phospholipid transport, mitochondrial-associated endoplasmic reticulum membrane (MAM) integrity, and lipid biosynthesis pathways. Protein-protein interaction network analyses identified FABP5 as a key molecular hub coordinating intracellular lipid trafficking and metabolic adaptation. Collectively, these multi-omics datasets establish that DED is characterized by ER-mitochondrial lipid crosstalk disruption and organelle stress signaling, providing mechanistic insights and therapeutic entry points for restoring ocular surface lipid homeostasis. Raw mass spectrometry data for both human and mouse samples have been deposited in the iProX database.","dates":{"publication":"Sat Apr 04 00:00:00 BST 2026"},"accession":"PXD076652","cross_references":{"TAXONOMY":["10090","9606"]}}