Myocyte Specific Upregulation of ACE2 in Cardiovascular Disease: Implications for SARS-CoV-2 mediated myocarditis.
Nathan R TuckerMark D ChaffinKenneth C BediIrinna PapangeliAmer-Denis AkkadAlessandro ArduiniSikander HayatGökcen EraslanChristoph MuusRoby P BhattacharyyaChristian M StegmannKenneth B MarguliesPatrick T EllinorPublished in: medRxiv : the preprint server for health sciences (2020)
Coronavirus disease 2019 (COVID-19) is a global pandemic caused by a novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). SARS-CoV-2 infection of host cells occurs predominantly via binding of the viral surface spike protein to the human angiotensin-converting enzyme 2 (ACE2) receptor. Hypertension and pre-existing cardiovascular disease are risk factors for morbidity from COVID-19, and it remains uncertain whether the use of angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB) impacts infection and disease. Here, we aim to shed light on this question by assessing ACE2 expression in normal and diseased human myocardial samples profiled by bulk and single nucleus RNA-seq.
Keyphrases
- angiotensin converting enzyme
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- angiotensin ii
- cardiovascular disease
- rna seq
- endothelial cells
- poor prognosis
- binding protein
- single cell
- induced pluripotent stem cells
- blood pressure
- induced apoptosis
- type diabetes
- pluripotent stem cells
- cell cycle arrest
- signaling pathway
- cell proliferation
- cell death
- long non coding rna
- transcription factor
- small molecule
- coronary artery disease
- protein protein
- african american
- dna binding