Evidence map›Paper›PMID 39702863›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Methods to Detect and Compare Cellular and Mitochondrial Changes in Senescent and Healthy Mesenchymal Stem Cells.

Afshin Samiminemati, Mohd Shahzaib, Claudia Moriello, Nicola Alessio, Domenico Aprile, Tiziana Squillaro, Giovanni Di Bernardo, Umberto Galderisi

Abstract read
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In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Polyphenol-Rich Extracts fromAntioxidants (Basel, Switzerland) · 2026
    Article
  2. 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.

Afshin Samiminemati *Department of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Mohd Shahzaib *Department of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Claudia MorielloDepartment of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Nicola AlessioDepartment of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Domenico AprileDepartment of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Tiziana SquillaroDepartment of Life Sciences, Health and Health Professions, Link Campus University, Rome, Italy.
Giovanni Di BernardoDepartment of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Umberto GalderisiDepartment of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy. umberto.galderisi@unicampania.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a multifaceted process marked by irreversible cell cycle arrest in response to stressors such as DNA damage, oxidative stress, and telomere shortening, leading to significant cellular and mitochondrial alterations. These changes impact mesenchymal stem cell (MSC) function, affecting their differentiation, self-renewal, and regenerative abilities. Senescent MSCs adopt the senescence-associated secretory phenotype (SASP), characterized by the secretion of pro-inflammatory factors that propagate senescence to neighboring cells. Key features of senescent MSCs include altered morphology, reduced proliferative and differentiation capacity, and changes in their secretome. Mitochondrial dysfunction plays a central role in this process, impairing stemness, increasing oxidative stress, and contributing to cellular aging by generating reactive oxygen species (ROS). The chapter provides an overview of various methods to analyze senescent cells, including techniques to detect changes in cell proliferation, DNA damage, apoptosis, and mitochondrial function. It also highlights assays for mitochondrial alterations such as fluorescent staining, membrane potential analysis, and mitophagy evaluation. These tools are essential for understanding the complex mechanisms of cellular senescence and mitochondrial dysfunction, offering insights into aging and potential therapeutic strategies.

Indexed as

Cellular SenescenceMesenchymal Stem CellsMitochondriaApoptosisCell DifferentiationCell ProliferationCells, CulturedDNA DamageHumansMembrane Potential, MitochondrialMitophagyOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesMesenchymal Stromal CellsMitochondria dysfunctionMitochondria morphologyMSCsSASPSenescence markers

Identifiers

PMID39702863

What Socratic holds

Textmetadata
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.