Lipids to the Rescue in Pulmonary Fibrosis: Biosynthesis, Bioenergetics, or Epigenetics? DOI
Manas Ranjan Gartia, Victor J. Thannickal

American Journal of Respiratory Cell and Molecular Biology, Год журнала: 2024, Номер 71(2), С. 143 - 145

Опубликована: Май 7, 2024

"Lipids to the Rescue in Pulmonary Fibrosis: Biosynthesis, Bioenergetics or Epigenetics?." American Journal of Respiratory Cell and Molecular Biology, 0(ja), pp.

Язык: Английский

Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development DOI Creative Commons
Justine Devulder

Chinese Medical Journal - Pulmonary and Critical Care Medicine, Год журнала: 2024, Номер 2(3), С. 133 - 141

Опубликована: Сен. 1, 2024

Язык: Английский

Процитировано

4

Aging-Associated Molecular Changes in Human Alveolar Type I Cells DOI

Xue Liu,

Xuexi Zhang, Jiurong Liang

и другие.

Deleted Journal, Год журнала: 2024, Номер 1(3), С. 10012 - 10012

Опубликована: Янв. 1, 2024

Human alveolar type I (AT1) cells are specialized epithelial that line the alveoli in lungs where gas exchange occurs. The primary function of AT1 is not only to facilitate efficient between air and blood lungs, but also contribute structural integrity maintain lung homeostasis. Aging has notable effects on structure, function, regenerative capacity human cells. However, our understanding molecular mechanisms driving these age-related changes remains limited. Leveraging a recent single-cell transcriptomics dataset we generated healthy identified series significant alterations from aged lungs. Notably, exhibited increased cellular senescence chemokine gene expression, alongside diminished features such as decreases cell junctions, endocytosis, pulmonary matrisome expression. Gene set analyses indicated were resistant apoptosis, crucial mechanism for turnover renewal cells, thereby ensuring function. Further research imperative fully elucidate impact indispensable developing effective therapies preserve promote aging.

Язык: Английский

Процитировано

3

Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis DOI Creative Commons
Guanling Huang, Gen Yan, Vrishika Kulur

и другие.

Deleted Journal, Год журнала: 2024, Номер 1(2), С. 10006 - 10006

Опубликована: Янв. 1, 2024

The molecular mechanisms that regulate progressive pulmonary fibrosis remain poorly understood. Type 2 alveolar epithelial cells (AEC2s) function as adult stem in the lung. We previously showed there is a loss of AEC2s and failure AEC2 renewal lungs idiopathic (IPF) patients. also reported beta-arrestins are key regulators fibroblast invasion, beta-arrestin 1 deficient mice exhibit decreased mortality, matrix deposition, increased lung bleomycin-induced fibrosis. However, role regeneration unclear. In this study, we investigated mechanism Arrestin beta (ARRB1) used conventional deletion well cell type-specific

Язык: Английский

Процитировано

2

Lipids to the Rescue in Pulmonary Fibrosis: Biosynthesis, Bioenergetics, or Epigenetics? DOI
Manas Ranjan Gartia, Victor J. Thannickal

American Journal of Respiratory Cell and Molecular Biology, Год журнала: 2024, Номер 71(2), С. 143 - 145

Опубликована: Май 7, 2024

"Lipids to the Rescue in Pulmonary Fibrosis: Biosynthesis, Bioenergetics or Epigenetics?." American Journal of Respiratory Cell and Molecular Biology, 0(ja), pp.

Язык: Английский

Процитировано

0