Intersection of immunometabolism and immunosenescence during aging

Kyoo a. Lee; Paul D. Robbins; Christina D. Camell

doi:10.1016/j.coph.2021.01.003

Intersection of immunometabolism and immunosenescence during aging

Kyoo a. Lee, Paul D. Robbins, Christina D. Camell

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Abstract

Aging is associated with the highest risk for morbidity and mortality to chronic or metabolic diseases, which are present in 50% of the elderly. Improving metabolic and immune function of the elderly would improve quality of life and reduce the risk for all other diseases. Tissue-resident macrophages and the NLRP3 inflammasome are established drivers of inflammaging and metabolic dysfunction. Energy-sensing signaling pathways connect sterile and metabolic inflammation with cellular senescence and tissue dysfunction. We discuss recent advances in the immunometabolism field. Common themes revealed by recent publications include the alterations in metabolic signaling (SIRTUIN, AMPK, or mTOR pathways) in aged immune cells, the impact of senescence on inflammaging and tissue dysfunction, and the age-related changes in metabolic tissues, especially adipose tissue, as an immunological organ. Promising gerotherapeutics are candidates to broadly target nutrient and energy sensing, inflammatory and senescence pathways, and have potential to improve healthspan and treat age-related diseases.

Original language	English (US)
Pages (from-to)	107-116
Number of pages	10
Journal	Current Opinion in Pharmacology
Volume	57
DOIs	https://doi.org/10.1016/j.coph.2021.01.003
State	Published - Apr 1 2021

Bibliographical note

Funding Information:
This work was supported by NIH grants RO1 AG063543 (PDR), RO1 AG063543-02S1 (PDR, CDC), P01 AG043376 (PDR), U19 AG056278 (PDR), P01 AG062413 (PDR), R01 AG069819 (PDR, CDC), R00 AG058800 (CDC), T32 AG029796 (KL), the Michael J. Fox Foundation for Parkinson's Research (PDR), the University of Minnesota Clinical and Translational Science Institute (PDR, CDC), and the Medical Discovery Team on the Biology of Aging (CDC, PDR). CDC also is supported by the Fesler-Lampert Chair in Aging Studies and the Glenn Foundation for Medical Research and AFAR Grants for Junior Faculty . These figures were created with BioRender.com . The authors thank Stephanie Cholensky for her comments and edits on the final manuscript.

Publisher Copyright:
© 2021

Keywords

AMPK-mTOR pathway
Adipose tissue
Aging
Immunometabolism
Inflammaging
Macrophage
NAD metabolism
NLRP3 inflammasome
SIRTUIN pathway

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10.1016/j.coph.2021.01.003

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title = "Intersection of immunometabolism and immunosenescence during aging",

abstract = "Aging is associated with the highest risk for morbidity and mortality to chronic or metabolic diseases, which are present in 50% of the elderly. Improving metabolic and immune function of the elderly would improve quality of life and reduce the risk for all other diseases. Tissue-resident macrophages and the NLRP3 inflammasome are established drivers of inflammaging and metabolic dysfunction. Energy-sensing signaling pathways connect sterile and metabolic inflammation with cellular senescence and tissue dysfunction. We discuss recent advances in the immunometabolism field. Common themes revealed by recent publications include the alterations in metabolic signaling (SIRTUIN, AMPK, or mTOR pathways) in aged immune cells, the impact of senescence on inflammaging and tissue dysfunction, and the age-related changes in metabolic tissues, especially adipose tissue, as an immunological organ. Promising gerotherapeutics are candidates to broadly target nutrient and energy sensing, inflammatory and senescence pathways, and have potential to improve healthspan and treat age-related diseases.",

keywords = "AMPK-mTOR pathway, Adipose tissue, Aging, Immunometabolism, Inflammaging, Macrophage, NAD metabolism, NLRP3 inflammasome, SIRTUIN pathway",

author = "Lee, {Kyoo a.} and Robbins, {Paul D.} and Camell, {Christina D.}",

note = "Funding Information: This work was supported by NIH grants RO1 AG063543 (PDR), RO1 AG063543-02S1 (PDR, CDC), P01 AG043376 (PDR), U19 AG056278 (PDR), P01 AG062413 (PDR), R01 AG069819 (PDR, CDC), R00 AG058800 (CDC), T32 AG029796 (KL), the Michael J. Fox Foundation for Parkinson's Research (PDR), the University of Minnesota Clinical and Translational Science Institute (PDR, CDC), and the Medical Discovery Team on the Biology of Aging (CDC, PDR). CDC also is supported by the Fesler-Lampert Chair in Aging Studies and the Glenn Foundation for Medical Research and AFAR Grants for Junior Faculty . These figures were created with BioRender.com . The authors thank Stephanie Cholensky for her comments and edits on the final manuscript. Publisher Copyright: {\textcopyright} 2021",

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doi = "10.1016/j.coph.2021.01.003",

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AU - Lee, Kyoo a.

AU - Robbins, Paul D.

AU - Camell, Christina D.

N1 - Funding Information: This work was supported by NIH grants RO1 AG063543 (PDR), RO1 AG063543-02S1 (PDR, CDC), P01 AG043376 (PDR), U19 AG056278 (PDR), P01 AG062413 (PDR), R01 AG069819 (PDR, CDC), R00 AG058800 (CDC), T32 AG029796 (KL), the Michael J. Fox Foundation for Parkinson's Research (PDR), the University of Minnesota Clinical and Translational Science Institute (PDR, CDC), and the Medical Discovery Team on the Biology of Aging (CDC, PDR). CDC also is supported by the Fesler-Lampert Chair in Aging Studies and the Glenn Foundation for Medical Research and AFAR Grants for Junior Faculty . These figures were created with BioRender.com . The authors thank Stephanie Cholensky for her comments and edits on the final manuscript. Publisher Copyright: © 2021

PY - 2021/4/1

Y1 - 2021/4/1

N2 - Aging is associated with the highest risk for morbidity and mortality to chronic or metabolic diseases, which are present in 50% of the elderly. Improving metabolic and immune function of the elderly would improve quality of life and reduce the risk for all other diseases. Tissue-resident macrophages and the NLRP3 inflammasome are established drivers of inflammaging and metabolic dysfunction. Energy-sensing signaling pathways connect sterile and metabolic inflammation with cellular senescence and tissue dysfunction. We discuss recent advances in the immunometabolism field. Common themes revealed by recent publications include the alterations in metabolic signaling (SIRTUIN, AMPK, or mTOR pathways) in aged immune cells, the impact of senescence on inflammaging and tissue dysfunction, and the age-related changes in metabolic tissues, especially adipose tissue, as an immunological organ. Promising gerotherapeutics are candidates to broadly target nutrient and energy sensing, inflammatory and senescence pathways, and have potential to improve healthspan and treat age-related diseases.

AB - Aging is associated with the highest risk for morbidity and mortality to chronic or metabolic diseases, which are present in 50% of the elderly. Improving metabolic and immune function of the elderly would improve quality of life and reduce the risk for all other diseases. Tissue-resident macrophages and the NLRP3 inflammasome are established drivers of inflammaging and metabolic dysfunction. Energy-sensing signaling pathways connect sterile and metabolic inflammation with cellular senescence and tissue dysfunction. We discuss recent advances in the immunometabolism field. Common themes revealed by recent publications include the alterations in metabolic signaling (SIRTUIN, AMPK, or mTOR pathways) in aged immune cells, the impact of senescence on inflammaging and tissue dysfunction, and the age-related changes in metabolic tissues, especially adipose tissue, as an immunological organ. Promising gerotherapeutics are candidates to broadly target nutrient and energy sensing, inflammatory and senescence pathways, and have potential to improve healthspan and treat age-related diseases.

KW - AMPK-mTOR pathway

KW - Adipose tissue

KW - Aging

KW - Immunometabolism

KW - Inflammaging

KW - Macrophage

KW - NAD metabolism

KW - NLRP3 inflammasome

KW - SIRTUIN pathway

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JO - Current Opinion in Pharmacology

JF - Current Opinion in Pharmacology

ER -

Intersection of immunometabolism and immunosenescence during aging

Abstract

Bibliographical note

Keywords

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