Evidence map›Paper›PMID 31900237›Full record

ArticleStem cell research & therapy2020

Alteration of fatty acid oxidation by increased CPT1A on replicative senescence of placenta-derived mesenchymal stem cells.

Jin Seok, Hyun Sook Jung, Sohae Park, Jung Ok Lee, Chong Jai Kim, Gi Jin Kim

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
20.0field-weighted citation impact, top 1% 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

25 citing papers in PubMed, 240 citations in OpenAlex.

  1. Article
  2. Review
  3. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
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  20. Rejuvenation ofFrontiers in pharmacology · 2021
    Article
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 at 4 institutions in 1 country.

Jin SeokDepartment of Biomedical Science, CHA University, 689, Sampyeong-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea.
Hyun Sook JungDepartment of Biomedical Science, CHA University, 689, Sampyeong-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea.
Sohae ParkDepartment of Biomedical Science, CHA University, 689, Sampyeong-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea.
Jung Ok LeeDepartment of Anatomy, Korea University College of Medicine, Seoul, Republic of Korea.
Chong Jai KimDepartment of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea.
Gi Jin KimDepartment of Biomedical Science, CHA University, 689, Sampyeong-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea. gjkim@cha.ac.kr.ORCID 0000-0002-2320-7157
CHA University · KRCHA University Bundang Medical Center · KRKorea University · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman placenta-derived mesenchymal stem cells (PD-MSCs) are powerful sources for cell therapy in regenerative medicine. However, a limited lifespan by senescence through mechanisms that are well unknown is the greatest obstacle. In the present study, we first demonstrated the characterization of replicative senescent PD-MSCs and their possible mitochondrial functional alterations.

methodsHuman PD-MSCs were cultured to senescent cells for a long period of time. The cells of before passage number 8 were early cells and after passage number 14 were late cells. Also, immortalized cells of PD-MSCs (overexpressed hTERT gene into PD-MSCs) after passage number 14 were positive control of non-senescent cells. The characterization and mitochondria analysis of PD-MSCs were explored with long-term cultivation.

resultsLong-term cultivation of PD-MSCs exhibited increases of senescent markers such as SA-β-gal and p21 including apoptotic factor, and decreases of proliferation, differentiation potential, and survival factor. Mitochondrial dysfunction was also observed in membrane potential and metabolic flexibility with enlarged mitochondrial mass. Interestingly, we founded that fatty acid oxidation (FAO) is an important metabolism in PD-MSCs, and carnitine palmitoyltransferase1A (CPT1A) overexpressed in senescent PD-MSCs. The inhibition of CPT1A induced a change of energy metabolism and reversed senescence of PD-MSCs.

conclusionsThese findings suggest that alteration of FAO by increased CPT1A plays an important role in mitochondrial dysfunction and senescence of PD-MSCs during long-term cultivation.

Indexed as

Carnitine O-PalmitoyltransferaseCell ProliferationCellular SenescenceFatty AcidsFemaleHumansMesenchymal Stem CellsMitochondriaOxidation-ReductionPlacentaPregnancyCarnitine O-PalmitoyltransferaseCPT1A protein, humanFatty AcidsCPT1AFatty acidMitochondriaPlacenta-derived mesenchymal stem cellSenescence

Identifiers

PMID31900237
PMCPMC6941254
OpenAlexW3000435216

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LicenceCC BY
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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.