Evidence map›Paper›PMID 37942323›Full record

ReviewFrontiers in immunology2023

From aging to long COVID: exploring the convergence of immunosenescence, inflammaging, and autoimmunity.

Ludmila Müller, Svetlana Di Benedetto

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Long COVID: Is mitochondria the target?Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Immunological biomarkers of aging.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  11. Observational
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
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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

2 authors at 1 institution in 1 country.

Ludmila MüllerMax Planck Institute for Human Development, Center for Lifespan Psychology, Berlin, Germany.
Svetlana Di BenedettoMax Planck Institute for Human Development, Center for Lifespan Psychology, Berlin, Germany.
Max Planck Institute for Human Development · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The process of aging is accompanied by a dynamic restructuring of the immune response, a phenomenon known as immunosenescence. This mini-review navigates through the complex landscape of age-associated immune changes, chronic inflammation, age-related autoimmune tendencies, and their potential links with immunopathology of Long COVID. Immunosenescence serves as an introductory departure point, elucidating alterations in immune cell profiles and their functional dynamics, changes in T-cell receptor signaling, cytokine network dysregulation, and compromised regulatory T-cell function. Subsequent scrutiny of chronic inflammation, or "inflammaging," highlights its roles in age-related autoimmune susceptibilities and its potential as a mediator of the immune perturbations observed in Long COVID patients. The introduction of epigenetic facets further amplifies the potential interconnections. In this compact review, we consider the dynamic interactions between immunosenescence, inflammation, and autoimmunity. We aim to explore the multifaceted relationships that link these processes and shed light on the underlying mechanisms that drive their interconnectedness. With a focus on understanding the immunological changes in the context of aging, we seek to provide insights into how immunosenescence and inflammation contribute to the emergence and progression of autoimmune disorders in the elderly and may serve as potential mediator for Long COVID disturbances.

Indexed as

Autoimmune DiseasesCOVID-19ImmunosenescenceAgedAgingAutoimmunityHumansInflammationPost-Acute COVID-19 Syndromeagingautoimmunityepigeneticsimmunosenescenceinflammaginglong COVIDSARS-CoV-2

Identifiers

PMID37942323
PMCPMC10628127
OpenAlexW4387900127

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.