Single-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy.

Ruben De Man, John E McDonough, Taylor S Adams, Fadi Nikola, Reina Rangel, Sabina Anderson, Edward P Manning, Juan Cala Garcia, Benjamin Moss, Alan Waich, Fernando Poli, Rafael Cardenas, Cristian Coarfa, Qi Song, Ziv Bar-Joseph, Bart M Vanaudenaerde, Wim A Wuyts, Laura Niklason, Micha Sam B Raredon, Xiting Yan, Ivan O Rosas, Naftali Kaminski

Section of Pulmonary, Critical Care, and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA.Section of Pulmonary, Critical Care, and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA. · pubmed

Paper

Abstract

Age is a major risk factor for lung disease. We characterized the changing cellular, transcriptional, and genomic landscape of human lung aging using single-cell RNA sequencing. We find that lung aging is cell-type dyssynchronous, with alveolar epithelial and endothelial cells exhibiting the greatest transcriptional changes. Among alveolar epithelial cells, aging is associated with a decreased relative proportion of surfactant-expressing SPC

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that lung aging is characterized by cell-type dyssynchrony and increased transcriptional entropy, particularly in alveolar epithelial and endothelial cells. This research is relevant as it explores the cellular and transcriptional changes associated with aging in the lungs, contributing to the understanding of the biological mechanisms underlying aging and age-related diseases.

Author of this paper? Send a correction.