Defying "IL-11ness" by inhibiting inflammation: Strategy for health and longevity

Hee-Hoon Kim; Vishwa Deep Dixit

doi:10.1016/j.cmet.2024.08.003

Defying "IL-11ness" by inhibiting inflammation: Strategy for health and longevity

Cell Metab. 2024 Sep 3;36(9):1911-1913. doi: 10.1016/j.cmet.2024.08.003.

Authors

Hee-Hoon Kim¹, Vishwa Deep Dixit²

Affiliations

¹ Department of Pathology, Yale School of Medicine, New Haven, CT 06520, USA; Department of Immunobiology and Comparative Medicine, Yale School of Medicine, New Haven, CT 06520, USA.
² Department of Pathology, Yale School of Medicine, New Haven, CT 06520, USA; Department of Immunobiology and Comparative Medicine, Yale School of Medicine, New Haven, CT 06520, USA; Yale Center for Research on Aging, New Haven, CT 06520, USA. Electronic address: vishwa.dixit@yale.edu.

PMID: 39232279
DOI: 10.1016/j.cmet.2024.08.003

Abstract

Organismal aging involves several hallmark pathways, including chronic inflammation and metabolic dysfunction. However, the origin of age-related inflammation is incompletely understood. In a recent study published in Nature,¹ Widjaja et al. show that blocking the age-related increase in IL-11 restores immune-metabolic homeostasis and extends healthspan and lifespan in mice.

MeSH terms

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

Substances

Interleukin-11