Evidence map›Paper›PMID 41935397›Full record

ArticleCurrent protein & peptide science2026

Marine-Derived Quinolinone CHNQD-00603 Triggers Autophagy via Suppressing the AKT/ERK/mTOR Pathway to Reverse Senescence and Restore Osteogenic Potential in Bone Marrow Mesenchymal Stem Cells.

Shengqian Li, Baoying Peng, Xiaoxia Yang, Wenhao Ren, Shaoming Li, Kai Sun, Keqian Zhi, Ling Gao, Jingjing Zheng

Abstract read
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In one paragraph

Article in Current protein & peptide science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Nutrition and Metabolism in Musculoskeletal Diseases.Current protein & peptide science · 2026
    Article
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

9 authors.

Shengqian LiDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Baoying PengDepartment of Pediatric Dentistry, Qingdao Stomatological Hospital Affiliated to Qingdao University, Qingdao, 266001, China.
Xiaoxia YangDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Wenhao RenDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Shaoming LiDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Kai SunDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Keqian ZhiDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Ling GaoDepartment of Oral and Maxillofacial Reconstruction, The Affiliated Hospital of Qingdao University, Qingdao, 266555, China.
Jingjing ZhengDepartment of Endodontics, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China.

Funding

Medical and Health Science and Technology Development Project of Shandong Province 202308021296National Natural Science Foundation of China 42176096Natural Science Foundation of Shandong Province ZR2021MD065, ZR2021MH305, ZR2022MH223State Administration of Traditional Chinese Medicine Science and Technology department coconstruction of science and technology project GZY-KJS-SD-2023-078TaiShan Scholars Foundation of Shandong Province tsqn202306397
6 · The paper itself

Abstract

introductionCellular senescence of Bone Marrow Mesenchymal Stem Cells (BMSCs) acts as a primary driver of age-related bone loss. This study aimed to investigate the anti-senescence potential of CHNQD-00603, a marine-derived quinolone derivative, and its underlying molecular mechanism in BMSCs.

methodsBMSCs isolated from Sprague-Dawley rats were induced to senesce using D-galactose and treated with CHNQD-00603. The study employed SA-β-gal staining, qRT-PCR, Western blotting, and transmission electron microscopy to evaluate cellular senescence, osteogenic differentiation, and autophagic flux. Key signaling pathways were analyzed through the phosphorylation status of AKT, ERK, and mTOR.

resultsCHNQD-00603 significantly reduced the proportion of SA-β-gal-positive cells (P < 0.001) and downregulated senescence markers p16 (P< 0.05) and p21 (P < 0.001). Concurrently, it restored osteogenic potential, increasing the expression of RUNX2 (P < 0.001), ALP (P < 0.01), OPN (P < 0.001), and OCN (P < 0.001). Mechanistically, CHNQD-00603 activated autophagy by inhibiting the AKT/ERK/mTOR pathway, as manifested by an increased LC3-II/LC3-I ratio, decreased p62 levels, and autophagosome accumulation. DISCUSSION: These findings highlight CHNQD-00603 as a dual regulator that suppresses senescence while promoting osteogenesis. Although the study is limited by a lack of in vivo validation, it effectively positions this marine-derived compound as a specific modulator of autophagy-dependent signaling.

conclusionCHNQD-00603 mitigates BMSC senescence and restores osteogenic capacity by activating AKT/ERK/mTOR-mediated autophagy, making it a promising therapeutic candidate for the treatment of age-related skeletal disorders.

Indexed as

AutophagyCellular SenescenceMesenchymal Stem CellsOsteogenesisQuinolonesAnimalsBone Marrow CellsCell DifferentiationCells, CulturedMAP Kinase Signaling SystemProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesmTOR protein, ratProto-Oncogene Proteins c-aktQuinolonesTOR Serine-Threonine KinasesautophagyBone marrow mesenchymal stem cellsmarine natural productsosteogenic differentiationosteoporosissenescence

Identifiers

PMID41935397

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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.