The inflammaging clock strikes IL-11!

Saad Khan; Veronica Chang; Daniel A Winer

doi:10.1016/j.immuni.2024.08.010

The inflammaging clock strikes IL-11!

Immunity. 2024 Sep 10;57(9):2010-2012. doi: 10.1016/j.immuni.2024.08.010.

Authors

Saad Khan¹, Veronica Chang², Daniel A Winer³

Affiliations

¹ Division of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON M5G 1L7, Canada.
² Division of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON M5G 1L7, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada.
³ Division of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON M5G 1L7, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada; Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; Department of Immunology, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address: dwiner@buckinstitute.org.

PMID: 39260354
PMCID: PMC11449161 (available on 2025-09-10)
DOI: 10.1016/j.immuni.2024.08.010

Abstract

Chronic inflammation is considered a hallmark of aging. In a recent issue of Nature, Widjaja et al. examined genetic and pharmacologic inhibition of interleukin (IL)-11 on aging pathology and found that inhibiting IL-11 signaling increases lifespan and healthspan in mice.

Publication types

Comment

MeSH terms

Aging* / immunology
Animals
Humans
Inflammation* / immunology
Interleukin-11* / immunology
Interleukin-11* / metabolism
Longevity / immunology
Mice
Signal Transduction* / immunology

Substances

Interleukin-11

Grants and funding

R01 DK128435/DK/NIDDK NIH HHS/United States