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RNA-seq profiling reveals different pathways between remodeled vessels and myocardium in hypertrophic cardiomyopathy
Annalinda Pisano1, Loredana Le Pera2,3, Raffaella Carletti4
1Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Rome, Italy.
Insights
Researchers uncovered distinct molecular pathways in the heart vessels and cells of hypertrophic cardiomyopathy (HCM) patients. This study sheds light on the molecular mechanisms behind coronary microvascular dysfunction (CMD) in HCM.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Coronary microvascular dysfunction (CMD) is a significant feature of hypertrophic cardiomyopathy (HCM), leading to myocardial ischemia and poor patient outcomes.
- The underlying molecular mechanisms of CMD in HCM remain largely unknown.
- Understanding these mechanisms is crucial for identifying therapeutic targets.
Purpose of the Study:
- To investigate the molecular pathways associated with microvessel remodeling in HCM.
- To identify differentially expressed genes (DEGs) in cardiomyocytes and arterioles of HCM patients.
- To compare transcriptome profiles between HCM patients and controls.
Main Methods:
- Utilized interventricular septum myectomies from obstructive HCM patients (n=20) and donor hearts (CTRL, n=7).
- Employed laser capture microdissection to isolate remodeled intramyocardial arterioles and cardiomyocytes.
- Performed next-generation sequencing to analyze transcriptome profiles.
Main Results:
- Identified 720 exclusive DEGs in HCM cardiomyocytes and 1315 exclusive DEGs in HCM arterioles.
- Gene ontology and pathway enrichment analyses revealed distinct molecular alterations in arterioles versus cardiomyocytes.
- Demonstrated unique pathway changes between remodeled arterioles and cardiomyocytes in HCM patients compared to controls.
Conclusions:
- Distinct molecular pathways exist between remodeled arterioles and cardiomyocytes in HCM patients at the transcriptome level.
- These findings provide novel insights into the pathogenesis of CMD in HCM.
- Further research into these pathways may lead to new therapeutic strategies for HCM.
Objective:
Coronary microvascular dysfunction (CMD) is a key pathophysiological feature of hypertrophic cardiomyopathy (HCM), contributing to myocardial ischemia and representing a critical determinant of patients' adverse outcome. The molecular mechanisms underlying the morphological and functional changes of CMD are still unknown. Aim of this study was to obtain insights on the molecular pathways associated with microvessel remodeling in HCM.
Methods:
Interventricular septum myectomies from patients with obstructive HCM (n = 20) and donors' hearts (CTRL, discarded for technical reasons, n = 7) were collected. Remodeled intramyocardial arterioles and cardiomyocytes were microdissected by laser capture and next-generation sequencing was used to delineate the transcriptome profile.
Results:
We identified 720 exclusive differentially expressed genes (DEGs) in cardiomyocytes and 1315 exclusive DEGs in remodeled arterioles of HCM. Performing gene ontology and pathway enrichment analyses, we identified selectively altered pathways between remodeled arterioles and cardiomyocytes in HCM patients and controls.
Conclusions:
We demonstrate the existence of distinctive pathways between remodeled arterioles and cardiomyocytes in HCM patients and controls at the transcriptome level.
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