Meshal Ansari

TL;DR: The data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

TL;DR: It is shown that aging leads to increased transcriptional noise, indicating deregulated epigenetic control, and Computational integration of the aging proteome with the single cell transcriptomes predicts the cellular source of regulated proteins and creates an unbiased reference map of the Aging lung.

TL;DR: A Krt8+ transitional stem cell state that precedes the regeneration of AT1 cells and persists in human lung fibrosis is uncovered and it is proposed that in lungs fibrosis, perturbed molecular checkpoints on the way to terminal differentiation can cause aberrant persistence of regenerative intermediate stem cell states.

TL;DR: Differences in the cell type-specific expression of mediators of SARS-CoV-2 viral entry may be responsible for aspects of COVID-19 epidemiology and clinical course, and point to putative molecular pathways involved in disease susceptibility and pathogenesis.

TL;DR: In this paper, cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues was assessed.