Evidence mapPaperPMID 39696575Full record

ReviewCell communication and signaling : CCS2024

Targeting cellular senescence in kidney diseases and aging: A focus on mesenchymal stem cells and their paracrine factors.

Seyyedeh Mina Hejazian, Seyyed Sina Hejazian, Seyyedeh Mina Mostafavi, Seyed Mahdi Hosseiniyan, Soheila Montazersaheb, Mohammadreza Ardalan, Sepideh Zununi Vahed, Abolfazl Barzegari

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Review
  2. SGLT2 Inhibition Attenuates Renal Tubular Senescence by Suppressing CTRP1-Mediated Glucotoxic Stress in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
    Review
  7. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. 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

8 authors.

Seyyedeh Mina HejazianKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyyed Sina HejazianKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyyedeh Mina MostafaviAyatollah Taleghani Hospital, Research Development Unit, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Seyed Mahdi HosseiniyanKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Soheila MontazersahebMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammadreza ArdalanKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sepideh Zununi VahedKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. sepide.zununi@gmail.com.
Abolfazl BarzegariDepartment of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. barzegari.abolfazl@gmail.com.

Funding

Tabriz University of Medical Sciences 72723
6 · The paper itself

Abstract

Cellular senescence is a phenomenon distinguished by the halting of cellular division, typically triggered by DNA injury or numerous stress-inducing factors. Cellular senescence is implicated in various pathological and physiological processes and is a hallmark of aging. The presence of accumulated senescent cells, whether transiently (acute senescence) or persistently (chronic senescence) plays a dual role in various conditions such as natural kidney aging and different kidney disorders. Elevations in senescent cells and senescence-associated secretory phenotype (SASP) levels correlate with decreased kidney function, kidney ailments, and age-related conditions. Strategies involving senotherapeutic agents like senolytics, senomorphics, and senoinflammation have been devised to specifically target senescent cells. Mesenchymal stem cells (MSCs) and their secreted factors may also offer alternative approaches for anti-senescence interventions. The MSC-derived secretome compromises significant therapeutic benefits in kidney diseases by facilitating tissue repair via anti-inflammatory, anti-fibrosis, anti-apoptotic, and pro-angiogenesis effects, thereby improving kidney function and mitigating disease progression. Moreover, by promoting the clearance of senescent cells or modulating their secretory profiles, MSCs could potentially reverse some age-related declines in kidney function.This review article intends to shed light on the present discoveries concerning the role of cellular senescence in kidney aging and diseases. Furthermore, it outlines the role of senotherapeutics utilized to alleviate kidney damage and aging. It also highlights the possible impact of MSCs secretome on mitigating kidney injury and prolonging lifespan across various models of kidney diseases as a novel senotherapy.

Indexed as

AgingKidney DiseasesMesenchymal Stem CellsSenescence-Associated Secretory PhenotypeAnimalsHumansMesenchymal Stem Cell TransplantationParacrine CommunicationSenotherapeuticsSenotherapeuticsAcute kidney injuryCellular senescenceChronic kidney diseaseKidney agingMesenchymal stem cellsSecretome of MSCs

Identifiers

PMID39696575
PMCPMC11657437

What Socratic holds

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LicenceCC BY
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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.