Evidence map›Paper›PMID 37821752›Full record

ReviewGeroScience2024

Autonomic nervous system imbalance during aging contributes to impair endogenous anti-inflammaging strategies.

Sergio Giunta, Shijin Xia, Giuseppe Pelliccioni, Fabiola Olivieri

Open access · hybridAbstract readReview
In one paragraph

Review in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The bidirectional mechanistic links between Alzheimer's disease and cardiovascular disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Distributed fMRI Patterns Coupled to Low-Frequency Cardiorespiratory Dynamics Provide Markers of Aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  10. Review
  11. Article
  12. CD21Frontiers in aging · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Age-related degradation of behavioral and network features ofbioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Sergio GiuntaCasa Di Cura Prof. Nobili (Gruppo Garofalo (GHC)), Castiglione Dei Pepoli, Bologna, Italy.
Shijin XiaDepartment of Geriatrics, Shanghai Institute of Geriatrics, Huadong Hospital, Fudan University, Shanghai, China.
Giuseppe PelliccioniUnit of Neurology, IRCCS INRCA, Ancona, Italy.
Fabiola OlivieriDepartment of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica Delle Marche, Via Tronto 10/A, 60126, Ancona, Italy. f.olivieri@univpm.it.ORCID 0000-0002-9606-1144
Fudan University · CNIstituti di Ricovero e Cura a Carattere Scientifico · ITMarche Polytechnic University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammaging refers to the age-related low grade, sterile, chronic, systemic, and long-lasting subclinical, proinflammatory status, currently recognized as the main risk factor for development and progression of the most common age-related diseases (ARDs). Extensive investigations were focused on a plethora of proinflammatory stimuli that can fuel inflammaging, underestimating and partly neglecting important endogenous anti-inflammaging mechanisms that could play a crucial role in such age-related proinflammatory state. Studies on autonomic nervous system (ANS) functions during aging highlighted an imbalance toward an overactive sympathetic nervous system (SNS) tone, promoting proinflammatory conditions, and a diminished parasympathetic nervous system (PNS) activity, playing anti-inflammatory effects mediated by the so called cholinergic anti-inflammatory pathway (CAP). At the molecular level, CAP is characterized by signals communicated via the vagus nerve (with the possible involvement of the splenic nerves) through acetylcholine release to downregulate the inflammatory actions of macrophages, key players of inflammaging. Notably, decreased vagal function and increased burden of activated/senescent macrophages (macrophaging) probably precede the development of several age-related risk factors and diseases, while increased vagal function and reduced macrophaging could be associated with relevant reduction of risk profiles. Hypothalamic-pituitary-adrenal axis (HPA axis) is another pathway related to ANS promoting some anti-inflammatory response mainly through increased cortisol levels. In this perspective review, we highlighted that CAP and HPA, representing broadly "anti-inflammaging" mechanisms, have a reduced efficacy and lose effectiveness in aged people, a phenomenon that could contribute to fuel inflammaging. In this framework, strategies aimed to re-balance PNS/SNS activities could be explored to modulate systemic inflammaging especially at an early subclinical stage, thus increasing the chances to reach the extreme limit of human lifespan in healthy status.

Indexed as

Hypothalamo-Hypophyseal SystemInflammationAgedAgingAnti-Inflammatory AgentsAutonomic Nervous SystemHumansPituitary-Adrenal SystemAnti-Inflammatory AgentsAnti-inflammagingAutonomic imbalanceCardiovascular-inflammagingCholinergic anti-inflammatory pathway (CAP)Diminished parasympathetic activityHPA axisIncreased sympathetic toneInflammagingMacrophaging

Identifiers

PMID37821752
PMCPMC10828245
OpenAlexW4387541081

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.