Evidence mapPaperPMID 41588428Full record

ArticleJournal of nanobiotechnology2026

Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.

Jiaming Bi, Yan Chai, Hong Wang, Jiawei Zeng, Xiaohao Liu, Mingyan Yao, Yunzhi Liu, Shuaimei Xu

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jiaming Bi *Department of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, China.
Yan Chai *Department of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, China.
Hong Wang *School of Laboratory Medicine and Biotechnology, Southern medical university, GuangZhou, Guangdong, China.
Jiawei ZengDepartment of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, China.
Xiaohao LiuDepartment of Periodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, China.
Mingyan YaoDepartment of Endocrinology, Central Hospital, Baoding No.1, Baoding, China.
Yunzhi LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, Guangdong, China. liuyz@smu.edu.cn.
Shuaimei XuDepartment of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, No. 366 Jiangnan Avenue South, Guangzhou, 510280, China. xushuaimei@smu.edu.cn.

Funding

Natural Science Foundation of Hebei Province H2023104011Science and Technology Projects in Guangzhou 2025A04J3462
6 · The paper itself

Abstract

Periodontitis is a chronic inflammatory condition affecting billions globally, posing a significant public health challenge due to its high prevalence and associated tooth loss. The inflammatory microenvironment engendered by periodontitis can induce cellular senescence and functional impairment in critical reparative cells, such as periodontal ligament stem cells (PDLSCs), severely compromising their osteogenic differentiation potential and thereby obstructing the regeneration and repair of periodontal tissues, particularly alveolar bone. Although existing fundamental treatments, including subgingival scaling, and surgical interventions can partially manage the disease, they exhibit notable limitations in eradicating deep-seated inflammation and effectively promoting structural bone regeneration. Consequently, there is an urgent need to develop novel biological treatment strategies aimed at reversing the senescent state of PDLSCs and enhancing their regenerative capacity. Flufenamic acid (FFA) is a widely utilized non-steroidal anti-inflammatory drug known for its notable anti-inflammatory and osteogenic properties. It holds significant potential for application in periodontal tissue engineering; however, its precise effects and underlying mechanisms remain inadequately understood. In this investigation, FFA effectively reversed the senescent state of periodontal ligament stem cells (PDLSCs), resulting in a marked down-regulation of pro-inflammatory, cellular senescence, and osteoclast differentiation-related markers, alongside an up-regulation of osteogenic differentiation-related markers. Furthermore, FFA significantly inhibited M1 polarization and osteoclast differentiation activity in macrophages and osteoclast precursor cells. Drug target screening and molecular docking analyses indicated that FFA mitigates PDLSC senescence and enhances their osteogenic capacity through activation of the SIRT1 signaling pathway. Additionally, this study employed the biological effects of M1 macrophage membranes to develop biomimetic hybrid nanovesicles (FFA@M1-LPs) designed to respond to inflammatory microenvironments. These findings suggest that FFA could be a promising new drug for periodontitis treatment and offer insights for developing drug delivery strategies to effectively regenerate periodontal tissue.

Indexed as

Biomimetic MaterialsCellular SenescencePeriodontitisSirtuin 1Stem CellsAnimalsCell DifferentiationHumansInflammationMiceOsteogenesisPeriodontal LigamentUp-RegulationSirtuin 1Anti-agingBone regenerationFlufenamic acidHybrid membrane nanovesiclesSIRT1

Identifiers

PMID41588428
PMCPMC12918139

What Socratic holds

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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 Socratic graph.