Evidence map›Paper›PMID 36198058›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2022

RNA-seq profiling reveals different pathways between remodeled vessels and myocardium in hypertrophic cardiomyopathy.

Annalinda Pisano, Loredana Le Pera, Raffaella Carletti, Bruna Cerbelli, Maria G Pignataro, Angelina Pernazza, Fabrizio Ferre, Maria Lombardi, Davide Lazzeroni, Iacopo Olivotto and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 3 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 3 countries.

Annalinda PisanoDepartment of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Rome, Italy.
Loredana Le PeraItalian National Institute of Health (ISS), Core Facilities, Rome, Italy.
Raffaella CarlettiDepartment of Translational and Precision Medicine, Sapienza University of Rome, Rome, Italy.
Bruna CerbelliDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.
Maria G PignataroDepartment of Chemistry and Drug Technologies, Sapienza University of Rome, Rome, Italy.
Angelina PernazzaDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.
Fabrizio FerreDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Bologna, Italy.
Maria LombardiCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Davide LazzeroniCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Iacopo OlivottoCardiomyopathy Unit, Careggi University Hospital, Florence, Italy.
Ornella E RimoldiNational Research Council (IBFM-CNR), Institute of Molecular Bioimaging and Physiology, Milan, Italy.
Chiara FoglieniCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Paolo G CamiciCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Giulia d'AmatiDepartment of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Rome, Italy.
Sapienza University of Rome · ITVita-Salute San Raffaele University · ITAzienda Ospedaliero-Universitaria Careggi · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITNational Institute of Statistics · ITNational Research Council · ITUniversity Foundation · BEUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCoronary 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.

methodsInterventricular 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.

resultsWe 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.

conclusionsWe demonstrate the existence of distinctive pathways between remodeled arterioles and cardiomyocytes in HCM patients and controls at the transcriptome level.

Indexed as

Cardiomyopathy, HypertrophicMyocardial IschemiaHumansMicrovesselsMyocardiumRNA-Seqcoronary microvascular remodelinghypertrophic cardiomyopathypathway enrichment analysesremodeled arterioles dissected

Identifiers

PMID36198058
PMCPMC9787970
OpenAlexW4302013405

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.