Mid-old cells are a potential target for anti-aging interventions in the elderly

Young Hwa Kim, Young-Kyoung Lee, Soon Sang Park, So Hyun Park, So Yeong Eom, Young-Sam Lee, Wonhee John Lee, Juhee Jang, Daeha Seo, Hee Young Kang, Jin Cheol Kim, Su Bin Lim, Gyesoon Yoon, Hong Seok Kim, Jang-Hee Kim () and Tae Jun Park ()
Additional contact information
Young Hwa Kim: Ajou University Medical Center
Young-Kyoung Lee: Ajou University Medical Center
Soon Sang Park: Ajou University Medical Center
So Hyun Park: Ajou University School of Medicine
So Yeong Eom: Ajou University Medical Center
Young-Sam Lee: Daegu Gyeongbuk Institute of Science & Technology
Wonhee John Lee: Daegu Gyeongbuk Institute of Science & Technology
Juhee Jang: Daegu Gyeongbuk Institute of Science & Technology
Daeha Seo: Daegu Gyeongbuk Institute of Science & Technology
Hee Young Kang: Ajou University Medical Center
Jin Cheol Kim: Ajou University Medical Center
Su Bin Lim: Ajou University Medical Center
Gyesoon Yoon: Ajou University Medical Center
Hong Seok Kim: College of Medicine, Inha University
Jang-Hee Kim: Ajou University Medical Center
Tae Jun Park: Ajou University Medical Center

Nature Communications, 2023, vol. 14, issue 1, 1-16

Abstract: Abstract The biological process of aging is thought to result in part from accumulation of senescent cells in organs. However, the present study identified a subset of fibroblasts and smooth muscle cells which are the major constituents of organ stroma neither proliferative nor senescent in tissues of the elderly, which we termed “mid-old status” cells. Upregulation of pro-inflammatory genes (IL1B and SAA1) and downregulation of anti-inflammatory genes (SLIT2 and CXCL12) were detected in mid-old cells. In the stroma, SAA1 promotes development of the inflammatory microenvironment via upregulation of MMP9, which decreases the stability of epithelial cells present on the basement membrane, decreasing epithelial cell function. Remarkably, the microenvironmental change and the functional decline of mid-old cells could be reversed by a young cell-originated protein, SLIT2. Our data identify functional reversion of mid-old cells as a potential method to prevent or ameliorate aspects of aging-related tissue dysfunction.

Date: 2023
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-023-43491-w Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-43491-w

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-43491-w

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().