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10.1038/s41420-025-02881-3 http://scihub22266oqcxt.onion/10.1038/s41420-025-02881-3 41331241!?!41331241 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41331241&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cell+Death+Discov 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41331241|t=2025. Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy |pdf=|usr=}}{{41331241}} gab.com Text Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy JO: Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=41331241 #FOAvip Fuchs endothelial corneal dystrophy (FECD) is the leading indication of corneal transplantation worldwide and the focus of pathogenesis has been on the corneal endothelium. Instead of cellular analysis, we aimed to identify the protein changes of aqueous humor (AH) in patients with FECD and investigate in more detail the relationship between AH and corneal endothelium. We collected 13 AH samples of 7 early/middle stage FECD patients and 6 control patients during routine cataract surgery. The proteomes of AH were profiled with the 4D label-free quantitative tandem mass spectrometry. Among 1613 identified proteins, 44 proteins exhibited above two-fold upregulation in the AH of FECD patients than control patients. Gene ontology (GO) analysis showed the enrichment of mitochondrial components, which were further validated by ELISA of mitochondrial proteins SLC25A3, PC, and PARK7. Moreover, immunofluorescence staining and ultrastructural observation were conducted in clinical specimens, mouse corneal endothelium and cultured human corneal endothelial cells (HCECs). The mitochondrial protein TOM20 was reduced in the FECD corneal endothelium, accompanied by damaged mitochondrial ejection. We next isolated extracellular vesicles by ultracentrifugation from HCECs and revealed that the mitochondria copy numbers were significantly increased in UVA-irradiated cells. Inhibition of exosome biogenesis aggravated cell death and mitochondrial membrane potential impairment in FECD endothelial cells. Taken together, our results provided novel insights into the proteome characterization of the AH from FECD patients and offered new perspective to deepen the impaired mitochondrial quality control in the pathogenesis of FECD. Twit Text FOAVip Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy ????Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=41331241 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41331241 #FOAvip English Wikipedia <ref>{{Cite pmid|41331241}}</ref> Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy #MMPMID41331241 Zhao C; Wang Q; Zhou Q; Wang Z; Yao S; Sang T; Duan H; Wu J; Zhong X; Sui X; Shi W; Wang T Cell Death Discov 2025[Dec]; ? (?): ? PMID41331241show ga Fuchs endothelial corneal dystrophy (FECD) is the leading indication of corneal transplantation worldwide and the focus of pathogenesis has been on the corneal endothelium. Instead of cellular analysis, we aimed to identify the protein changes of aqueous humor (AH) in patients with FECD and investigate in more detail the relationship between AH and corneal endothelium. We collected 13 AH samples of 7 early/middle stage FECD patients and 6 control patients during routine cataract surgery. The proteomes of AH were profiled with the 4D label-free quantitative tandem mass spectrometry. Among 1613 identified proteins, 44 proteins exhibited above two-fold upregulation in the AH of FECD patients than control patients. Gene ontology (GO) analysis showed the enrichment of mitochondrial components, which were further validated by ELISA of mitochondrial proteins SLC25A3, PC, and PARK7. Moreover, immunofluorescence staining and ultrastructural observation were conducted in clinical specimens, mouse corneal endothelium and cultured human corneal endothelial cells (HCECs). The mitochondrial protein TOM20 was reduced in the FECD corneal endothelium, accompanied by damaged mitochondrial ejection. We next isolated extracellular vesicles by ultracentrifugation from HCECs and revealed that the mitochondria copy numbers were significantly increased in UVA-irradiated cells. Inhibition of exosome biogenesis aggravated cell death and mitochondrial membrane potential impairment in FECD endothelial cells. Taken together, our results provided novel insights into the proteome characterization of the AH from FECD patients and offered new perspective to deepen the impaired mitochondrial quality control in the pathogenesis of FECD. ?Blockade of mitochondrial components release by exosome pathway promot(epmc).pdf DeepDyve Pubget Overpricing