ArticleScientific reports2025
Alteration in Golgi apparatus fragmentation related genes in human dilated cardiomyopathy.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Organelle network dysfunction in primary cardiomyopathy: An integrated perspective on pathogenesis and therapeutics.Journal of molecular and cellular cardiology plus · 2026Review
- TMEM87a Maintains Cardiomyocyte Integrity by Limiting Ferroptosis in Dilated Cardiomyopathy.Annals of the New York Academy of Sciences · 2026Article
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
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7 authors.
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Abstract
The Golgi apparatus (GA) plays a main role in the protein secretory pathway. Previously, we described a greater GA vesicle density in patients with dilated cardiomyopathy (DCM), as well as an increase in natriuretic peptide (NP) levels inside these vesicles. GA fragmentation could increase the rate of protein transport; for this reason, we aimed to delve deeper into these GA vesicle density alterations by studying the expression of genes related to GA architecture in DCM and its relationship with NP levels. We performed RNA-seq analysis on explanted hearts from DCM patients (n = 13) and control (CNT) individuals (n = 10). We detected alterations in molecules related to the structure and positioning of GA, highlighting the decrease in GM130 levels and increase in the p-GM130/GM130 ratio (p < 0.05) observed via Western blotting (DCM, n = 23; CNT, n = 7) and their correlation with NT-proBNP levels (r = - 0.473, p < 0.05; r = 0.455, p < 0.05; respectively). We also observed an upregulation of genes involved in anterograde transport and a downregulation of genes involved in retrograde transport. Moreover, we visualized GA fragmentation in doxorubicin-induced DCM in AC16 cells via immunofluorescence (70.2% of the cells had fragmented GA, p < 0.05) and corroborated the downregulation of GOLGA2 and the increase in NP levels observed in human tissue. Our results revealed dysregulation of genes that maintain GA structure, suggesting that GA fragmentation occurs in DCM patients. Therefore, the imbalance between anterograde and retrograde transport could also contribute to this situation and to increased formation of transport vesicles.
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