Evidence map›Paper›PMID 42909967›Full record

ArticleTheranostics2026

ARG2 drives osteoblast senescence by repressing mitophagy via the IκB-NF-κB-TXN2 signaling axis: implications for age-associated osteoporosis.

Jinli Li, Liyao Zhang, Yuanyuan Ren, Junxuan Wang, Pan Zhang, Qianran Shen, Yaqi Wang, Yi Yu, Zi Cheng, Qiang Wang and 2 more

Abstract read
In one paragraph

Article in Theranostics, 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

12 authors.

Jinli LiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Liyao ZhangKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Yuanyuan RenKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Junxuan WangSchool of Medicine, Northwest University, Xi'an, Shaanxi 710069, China.
Pan ZhangKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Qianran ShenKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Yaqi WangKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Yi YuKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.
Zi ChengSchool of Medicine, Northwest University, Xi'an, Shaanxi 710069, China.
Qiang WangDepartment of Orthopaedics, Shenmu Hospital, The Affiliated Shenmu Hospital of Northwest University, Guangming Road, Shenmu, China.
Haiying WangDepartment of Science and Education, Shenmu Hospital, The Affiliated Shenmu Hospital of Northwest University, Shenmu, China.
Yuyan XiongKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, College of Life Sciences, Northwest University, Xi'an, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rationale: Age-associated osteoporosis (AAOP) is characterized by progressive bone loss that can be driven by impaired osteoblast function and increased cellular senescence. However, the molecular mechanisms driving osteoblast senescence during aging remain incompletely understood. In this study, we aim to investigate the role of arginase 2 (ARG2) and its underlying mechanisms in osteoblast senescence and AAOP. Methods: AAOP were assessed in D-galactose-induced aging mice, naturally aged mice, and osteoblast-specific ARG2 knockout mice. Results: We observed that ARG2 expression was markedly elevated in senescent osteoblasts and aged mice with osteoporosis. Osteoblast-specific deletion of ARG2 alleviated age-related bone loss, improved trabecular bone microarchitecture, and reduced osteoblast senescence Conclusion: ARG2 plays a pivotal role in osteoblast senescence and the development of AAOP by inducing mitochondrial oxidative stress and mitophagy dysfunction through the IκBα/NF-κB/HDAC9/TXN2 signaling axis. Targeting ARG2 may offer a promising therapeutic approach for AAOP prevention and treatment.

Indexed as

Cellular SenescenceMitophagyNF-kappa BOsteoblastsOsteoporosisAgingAnimalsGalactoseHumansI-kappa B ProteinsMaleMiceMice, KnockoutMitochondriaOxidative StressSignal TransductionGalactoseI-kappa B ProteinsNF-kappa BArginase 2mitochondrial oxidative stressmitophagyosteoblast senescencesenile osteoporosis

Identifiers

PMID42909967
PMCPMC13684819

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.