Evidence map›Paper›PMID 40627177›Full record

ReviewClinical and experimental medicine2025

Applications of CRISPR-Cas9 in mitigating cellular senescence and age-related disease progression.

Alireza Azani, Malihe Sharafi, Reyhaneh Doachi, Sama Akbarzadeh, Parsa Lorestani, Arash Haji Kamanaj Olia, Zahra Zahed, Hossein Gharedaghi, Haniyeh Ghasrsaz, Hassan Foroozand and 3 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

13 authors.

Alireza Azani *Department of Medical Genetic, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Malihe Sharafi *Department of Biology, Faculty of Basic Science, Azarbaijan Shahid Madani University, Tabriz, Iran.
Reyhaneh Doachi *Department of Medical Genetics, School of Medicine, Tehran University of Medical Science, Tehran, Iran.
Sama AkbarzadehDepartment of Biophysics, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Parsa LorestaniStudents Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Arash Haji Kamanaj OliaDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Zahra ZahedDepartment of Medical Sciences, Ardabil University of Medical Sciences, Ardabil, Iran.
Hossein GharedaghiSchool of Medicine, Zanjan University of Medical Science, Zanjan, Iran.
Haniyeh GhasrsazMazandaran University of Medical Sciences, Mazandaran, Iran.
Hassan ForoozandStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Hossein RahimiDalian Medical University, Dalian, China.
Safa TahmasebiStudents Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Safa.tahmasebi@sbmu.ac.ir.
Qumars BehfarSchool of Cardiovascular and Metabolic Health, University of Glasgow, Elizabeth University Hospital, Glasgow, Queen, UK. q_behfar@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a multifaceted process influenced by many elements. During cell division, the repetitive DNA sequences at the ends of chromosomes called telomeres protect them from degradation. Telomeres shorten alongside each cell division, eventually contributing to cellular senescence and aging. Telomerase as an enzyme has a role in the maintenance of telomere length. Reduced function of telomerase is linked to acceleration of aging and age-related diseases. By affecting cellular function, mutations in particular genes can cause aging. Genes involved in DNA repair, cellular metabolism, and inflammation play the key roles in this process. Accumulated mutations result in cellular dysfunction and age-related diseases over time. Epigenetic changes are the modifications that impact gene expression without altering the DNA sequence. Lifestyle factors (diet, exercise, stress) and environmental influences (toxins, trauma) can cause epigenetic alterations. DNA methylation as well as histone modifications are examples of epigenetic alterations. They influence how cells work and are essential to the aging process. Understanding these molecular mechanisms is essential for developing interventions to promote healthy aging and prevent age-related diseases. This paper explores the potential of CRISPR/Cas9 as a gene-editing tool to target these mechanisms and mitigate age-related conditions, ultimately enhancing longevity and quality of life.

Indexed as

AgingCellular SenescenceCRISPR-Cas SystemsGene EditingAnimalsDisease ProgressionEpigenesis, GeneticHumansTelomeraseTelomeraseAgingCRISPR-Cas9Gene editingMolecular and cellular mechanism

Identifiers

PMID40627177
PMCPMC12238200

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Registered trials

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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.