Evidence map›Paper›PMID 41727272›Full record

ArticleBioactive materials2026

A mitochondria-targeted nanoantioxidant restores alveolar bone homeostasis in periodontitis by quenching ROS and suppressing the cGAS-STING pathway.

Ning Huang, Lingyan Cao, Yue Xu, Lisha Pan, Ao Zheng, Xiao Wang, Xinquan Jiang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
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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

7 authors.

Ning HuangDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.
Lingyan CaoDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.
Yue XuShanghai Stomatological Hospital, Fudan University, 166 Hechuan Road, Shanghai, 201103, China.
Lisha PanDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.
Ao ZhengDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.
Xiao WangDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.
Xinquan JiangDepartment of Prosthodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, 639 Zhizaoju Road, Shanghai, 200011, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolonged periodontal inflammation and progressive alveolar bone loss are typical manifestations of periodontitis. Antioxidative therapies targeting the central role of reactive oxygen species (ROS) have been explored, but lack of subcellular specificity limits efficacy. Mitochondria function as an upstream redox hub that drives oxidative stress, inflammatory responses, and alveolar bone resorption, making mitochondrial redox modulation a promising yet underexplored strategy for periodontitis therapy. Herein, we developed a mitochondria-targeted, redox-responsive nanocomposite (TC/pSeSe) that enables programmable redox modulation of the pathological periodontal microenvironment. The antioxidative core consists of a ROS-responsive diselenide-containing copolymer (pSeSe) capable of selenium release, while the triphenylphosphine/chitosan (TC) coating confers mitochondrial-targeted, controlled redox activity, mucosal retention and cationic antibacterial properties. With preferential mitochondrial localization, TC/pSeSe undergoes diselenide bond cleavage and selenium release under oxidative stress, thereby restoring mitochondrial redox homeostasis and attenuating downstream mitochondrial DNA (mtDNA)-cGAS-STING-mediated inflammatory signaling. Through combined ROS scavenging and selenium-mediated support, TC/pSeSe mitigates ferroptosis in a partially glutathione peroxidase 4 (GPX4)-dependent manner and restores osteogenic potential in bone marrow-derived stem cells. In parallel, TC/pSeSe exhibits antibacterial activity against periodontal pathogens through combined selenium and the cationic TC coating functionalities.

Indexed as

cGAS-STINGMitochondria-targetedNanoantioxidantOxidative stressPeriodontitis

Identifiers

PMID41727272
PMCPMC12918178

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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.