Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences
Authors' conclusion
The unique nature of this human coronary biorepository with samples ranging from entirely normal to mature pre-clinical atherosclerotic plaque facilitated prediction of molecular disease progression and identification of several potential transcriptional regulators for further evaluation as potential novel targets to interrupt early initiation and progression of atherosclerotic coronary disease.
Study context
- Population
- Young adults who died of trauma with no ante mortem suspicion of coronary disease; proximal coronary arterial samples56% with pre-clinical atherosclerosis
- Participants
- 322 adults
- Outcome
- Proteomic latent features (LFs) and molecular disease progression
Methodological detailsproteomic analysis, RNA sequencing, arterial organoid model
- Proteomic analysis
- RNA sequencing
- Arterial organoid model
Main finding
As reported in the abstract
- Four proteomic latent features (LFs) (100 signature proteins/LF) showed distinct patterns with disease progression
- False discovery rate (FDR) P < .01
- Early changes: dramatic declines in mitochondrial energy biosynthesis proteins, vascular unit activation (incl. pericytes), neurovascular and neuroimmune modulation
- all FDR P < .01
- Public single-cell RNA sequencing (RNASeq) validated the LFs and several likely master transcriptional regulators
- all P < .01
- MLXIPL manipulation in arterial cell organoids changed expression of proteins of its two targeted LFs
- P = .0003 and P < .00001
Original publication
Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences. Eur Heart J. Published 12 May 2026. doi:10.
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