Evidence map›Paper›PMID 39135295›Full record

ReviewAging cell2024

Aging-associated atrial fibrillation: A comprehensive review focusing on the potential mechanisms.

Meng-Fei Wang, Can Hou, Fang Jia, Cheng-Hao Zhong, Cong Xue, Jian-Jun Li

Abstract readReview
In one paragraph

Review in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Understanding the Diseased Atria.Physiology (Bethesda, Md.) · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. MATR3 regulates METTL3-Mediated mJournal of bioenergetics and biomembranes · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Atrial fibrillation and flutter in the Eastern Mediterranean: burden, disparities, and risk factor contributions from 1990 to 2021.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025
    Article
  18. 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

6 authors.

Meng-Fei WangThe Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou, China.ORCID 0009-0004-7336-3651
Can HouThe Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou, China.
Fang JiaThe Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou, China.
Cheng-Hao ZhongThe Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou, China.
Cong XueThe Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou, Changzhou, China.
Jian-Jun LiState Key Laboratory of Cardiovascular Diseases, Fu Wai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Funding

Changzhou Key Medical Discipline CZXK202202Changzhou Sci&Tech Program CJ20235085Changzhou Sci&Tech Program CJ20235088
6 · The paper itself

Abstract

Atrial fibrillation (AF) has been receiving a lot of attention from scientists and clinicians because it is an extremely common clinical condition. Due to its special hemodynamic changes, AF has a high rate of disability and mortality. So far, although AF has some therapeutic means, it is still an incurable disease because of its complex risk factors and pathophysiologic mechanisms, which is a difficult problem for global public health. Age is an important independent risk factor for AF, and the incidence of AF increases with age. To date, there is no comprehensive review on aging-associated AF. In this review, we systematically discuss the pathophysiologic evidence for aging-associated AF, and in particular explore the pathophysiologic mechanisms of mitochondrial dysfunction, telomere attrition, cellular senescence, disabled macroautophagy, and gut dysbiosis involved in recent studies with aging-associated AF. We hope that by exploring the various dimensions of aging-associated AF, we can better understand the specific relationship between age and AF, which may be crucial for innovative treatments of aging-associated AF.

Indexed as

AgingAtrial FibrillationAnimalsCellular SenescenceHumansMitochondriaagingatrial fibrillationmechanisms

Identifiers

PMID39135295
PMCPMC11464128

What Socratic 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 Socratic graph.