Evidence map›Paper›PMID 28924347›Full record

ReviewInternational journal of nanomedicine2017

The mechanisms of graphene-based materials-induced programmed cell death: a review of apoptosis, autophagy, and programmed necrosis.

Lingling Ou, Shaoqiang Lin, Bin Song, Jia Liu, Renfa Lai, Longquan Shao

Open access · goldAbstract readReview
In one paragraph

Review in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
10.1field-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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 194 citations in OpenAlex.

  1. Pooled it
  2. Review
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  13. Ferroptosis in Cancer: Mechanism and Therapeutic Potential.International journal of molecular sciences · 2025
    Review
  14. Electrostrategies in orthopaedic research.Biomaterials translational · 2025
    Article
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  16. Review
  17. Article
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23 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Lingling OuDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Shaoqiang LinDepartment of Stomatology, the First Affiliated Hospital of Jinan University, Guangzhou, People's Republic of China.
Bin SongDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Jia LiuDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Renfa LaiDepartment of Stomatology, the First Affiliated Hospital of Jinan University, Guangzhou, People's Republic of China.
Longquan ShaoDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
First Affiliated Hospital of Jinan University · CNNanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graphene-based materials (GBMs) are widely used in many fields, including biomedicine. To date, much attention had been paid to the potential unexpected toxic effects of GBMs. Here, we review the recent literature regarding the impact of GBMs on programmed cell death (PCD). Apoptosis, autophagy, and programmed necrosis are three major PCDs. Mechanistic studies demonstrated that the mitochondrial pathways and MAPKs (JNK, ERK, and p38)- and TGF-β-related signaling pathways are implicated in GBMs-induced apoptosis. Autophagy, unlike apoptosis and necroptosis which are already clear cell death types, plays a vital pro-survival role in cell homeostasis, so its role in cell death should be carefully considered. However, GBMs always induce unrestrained autophagy accelerating cell death. GBMs trigger autophagy through inducing autophagosome accumulation and lysosome impairment. Mitochondrial dysfunction, ER stress, TLRs signaling pathways, and p38 MAPK and NF-κB pathways participate in GBMs-induced autophagy. Programmed necrosis can be activated by RIP kinases, PARP, and TLR-4 signaling in macrophages after GBMs exposure. Though apoptosis, autophagy, and necroptosis are distinguished by some characteristics, their numerous signaling pathways comprise an interconnected network and correlate with each other, such as the TLRs, p53 signaling pathways, and the Beclin-1 and Bcl-2 interaction. A better understanding of the mechanisms of PCD induced by GBMs may allow for a thorough study of the toxicology of GBMs and a more precise determination of the consequences of human exposure to GBMs. These determinations will also benefit safety assessments of the biomedical and therapeutic applications of GBMs.

Indexed as

AnimalsApoptosisAutophagyGraphiteHumansMacrophagesMitochondriaNecrosisNF-kappa BSignal TransductionTransforming Growth Factor betaGraphiteNF-kappa BTransforming Growth Factor betacell toxicitygraphene based materialsmechanismsprogrammed cell death

Identifiers

PMID28924347
PMCPMC5595361
OpenAlexW2752862273

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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 OpenQuestion graph.