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Cell non-autonomous regulation of health and longevity

Miller, Hillary A, Dean, Elizabeth S, Pletcher, Scott D, Leiser, Scott F·2020·eLife
DOI 10.7554/elife.62659PMC PMC7728442
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Abstract

As the demographics of the modern world skew older, understanding and mitigating the effects of aging is increasingly important within biomedical research. Recent studies in model organisms demonstrate that the aging process is frequently modified by an organism’s ability to perceive and respond to changes in its environment. Many well-studied pathways that influence aging involve sensory cells, frequently neurons, that signal to peripheral tissues and promote survival during the presence of stress. Importantly, this activation of stress response pathways is often sufficient to improve health and longevity even in the absence of stress. Here, we review the current landscape of research highlighting the importance of cell non-autonomous signaling in modulating aging from C. elegans to mammals. We also discuss emerging concepts including retrograde signaling, approaches to mapping these networks, and development of potential therapeutics.

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  • Aging involves deficiencies in neural, neuroendocrine and hormonal signaling pathways, including the adrenergic, dopaminergic, insulin/IGF1-based and renin-angiotensin systems, as well as sex hormones commensurate with the loss of reproductive functions.

    “Thus, aging involves deficiencies in neural, neuroendocrine and hormonal signaling pathways, including the adrenergic, dopaminergic, insulin/IGF1-based and renin-angiotensin systems, as well as sex hormones commensurate with the loss of reproductive functions 134,228 .”

    From Hallmarks of aging: An expanding universe (2023) · cites this paper as [228]

    The Mammals section links age-related inflammation to reduced GnRH release and discusses insulin and dopamine signaling in longevity. It does not establish that aging generally causes deficiencies across all the listed pathways; the passages found do not address renin–angiotensin signaling or declining sex hormones. The paper also reports that reduced insulin/IGF-1 signaling can extend lifespan, rather than presenting it as an age-related deficiency. (LLM, conf=0.86)

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Metadata

Authors
Miller, H. A., Dean, E. S., Pletcher, S. D., & Leiser, S. F.
Affiliations
  • Cellular and Molecular Biology Graduate Program, University of Michigan, Ann Arbor, United States
  • Molecular & Integrative Physiology Department, University of Michigan, Ann Arbor, United States
ORCID
Venue
eLife
Publisher
eLife Sciences Publications, Ltd
Published
2020-12-10
Volume
9
ISSN
2050-084X
DOI
10.7554/elife.62659
PMC
PMC7728442
Cited by
102
References
27
Language
en
Licence
Funders
  • National Institutes of Health (R01AG058717, R01AG059583, F31AG060663)
  • National Science Foundation

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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