Evidence map›Paper›PMID 32273566›Full record

ArticleExperimental & molecular medicine2020

Pharmacological inhibition of mTOR attenuates replicative cell senescence and improves cellular function via regulating the STAT3-PIM1 axis in human cardiac progenitor cells.

Ji Hye Park, Na Kyoung Lee, Hye Ji Lim, Seung Taek Ji, Yeon-Ju Kim, Woong Bi Jang, Da Yeon Kim, Songhwa Kang, Jisoo Yun, Jong Seong Ha and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  10. Expression of PIM1/ASK1 Molecular Pathway Related Genes in Ischemic Cardiomyopathy.Cardiovascular & hematological disorders drug targets · 2025
    Article
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  19. microRNA-449a reduces growth hormone-stimulated senescent cell burden through PI3K-mTOR signaling.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Ji Hye ParkLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Na Kyoung LeeLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Hye Ji LimLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Seung Taek JiLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Yeon-Ju KimLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Woong Bi JangLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Da Yeon KimLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Songhwa KangLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Jisoo YunLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Jong Seong HaLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.ORCID http://orcid.org/0000-0001-5804-2607
Hyungtae KimDepartment of Thoracic and Cardiovascular Surgery, Pusan National University Yangsan Hospital, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea.
Dongjun LeeDepartment of Convergence Medical Science, Pusan National University School of Medicine, Yangsan, 50612, Republic of Korea. lee.dongjun@pusan.ac.kr.ORCID http://orcid.org/0000-0001-6828-401X
Sang Hong BaekLaboratory of Cardiovascular Disease, Division of Cardiology, School of Medicine, The Catholic University of Korea, Seoul, 137-040, Republic of Korea. whitesh@catholic.ac.kr.
Sang-Mo KwonLaboratory of Regenerative Medicine and Stem Cell Biology, Department of Physiology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 50612, Republic of Korea. smkwon323@pusan.ac.kr.
Pusan National University · KRPusan National University Yangsan Hospital · KRCatholic University of Korea · KRKorea Institute of Toxicology · KR

Funding

National Research Foundation of Korea (NRF) 2018R1A2B6006380National Research Foundation of Korea (NRF) 2018R1C1B6001290National Research Foundation of Korea (NRF) NRF-2015R1A5A2009656National Research Foundation of Korea (NRF) NRF-2018R1A2B6006380
6 · The paper itself

Abstract

The mammalian target of rapamycin (mTOR) signaling pathway efficiently regulates the energy state of cells and maintains tissue homeostasis. Dysregulation of the mTOR pathway has been implicated in several human diseases. Rapamycin is a specific inhibitor of mTOR and pharmacological inhibition of mTOR with rapamycin promote cardiac cell generation from the differentiation of mouse and human embryonic stem cells. These studies strongly implicate a role of sustained mTOR activity in the differentiating functions of embryonic stem cells; however, they do not directly address the required effect for sustained mTOR activity in human cardiac progenitor cells. In the present study, we evaluated the effect of mTOR inhibition by rapamycin on the cellular function of human cardiac progenitor cells and discovered that treatment with rapamycin markedly attenuated replicative cell senescence in human cardiac progenitor cells (hCPCs) and promoted their cellular functions. Furthermore, rapamycin not only inhibited mTOR signaling but also influenced signaling pathways, including STAT3 and PIM1, in hCPCs. Therefore, these data reveal a crucial function for rapamycin in senescent hCPCs and provide clinical strategies based on chronic mTOR activity.

Indexed as

Cell DifferentiationCell ProliferationCells, CulturedCellular SenescenceComputational BiologyGene Expression ProfilingHumansMyoblasts, CardiacProto-Oncogene Proteins c-pim-1Signal TransductionSirolimusSTAT3 Transcription FactorStem CellsTOR Serine-Threonine KinasesMTOR protein, humanPIM1 protein, humanProto-Oncogene Proteins c-pim-1SirolimusSTAT3 protein, humanSTAT3 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID32273566
PMCPMC7210934
OpenAlexW3016197213

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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.