Targeting endothelial to mesenchymal transition in atherosclerosis: invited editorial
This editorial refers to ‘Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition’ by Z. Guo et al., https://doi.org/10.1093/cvr/cvag078.Despite substantial advances in lipid-lowering therapies, residual cardiovascula...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article (Journal) Editorial |
| Language: | English |
| Published: |
June 2026
|
| In: |
Cardiovascular research
Year: 2026, Volume: 122, Issue: 9, Pages: 1119-1121 |
| ISSN: | 1755-3245 |
| DOI: | 10.1093/cvr/cvag097 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1093/cvr/cvag097
|
| Author Notes: | Giorgia Ciliberti, Marco Sachse, and Konstantinos Stellos |
| Summary: | This editorial refers to ‘Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition’ by Z. Guo et al., https://doi.org/10.1093/cvr/cvag078.Despite substantial advances in lipid-lowering therapies, residual cardiovascular risk remains high in patients with atherosclerotic cardiovascular disease, particularly in patients with acute coronary syndromes.1-3 A central unresolved question is how metabolic stress is translated into durable endothelial reprogramming that promotes atherosclerotic plaque instability, leading to acute coronary syndromes, stroke, or acute limb ischaemia. Endothelial-to-mesenchymal transition (EndMT) is a dynamic process in which endothelial cells progressively lose junctional integrity and canonical markers while acquiring a mesenchymal phenotype.4,5 Although physiologically required during development, aberrant EndMT is implicated in cardiovascular disease—including fibrosis, pulmonary hypertension, and atherosclerosis—where its extent correlates with plaque expansion and instability. Together, these observations define EndMT as a maladaptive endothelial reprogramming process; however, the upstream signals that metabolically encode this phenotypic switch remain poorly defined.4,5 |
|---|---|
| Item Description: | Online veröffentlicht: 16. Juni 2026 Gesehen am 23.07.2026 |
| Physical Description: | Online Resource |
| ISSN: | 1755-3245 |
| DOI: | 10.1093/cvr/cvag097 |