Evidence map›Paper›PMID 42875724›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Yoda1-Functionalized Nanozymes Coordinate Piezo1 Activation and Mitochondrial Protection to Reprogram the Diabetic Osteoimmune Micromilieu and Promote Vascularized Bone Repair.

Qing-Song Deng, Ang Wang, Ren Zhang, Xu-Ran Li, Po-Lin Liu, Shu-Hang He, Zi-Yin Han, Zhi-Han Shen, Zhan-Ying Wei, Chang-Ru Zhang and 7 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

17 authors.

Qing-Song Deng *Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ang Wang *Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ren Zhang *Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xu-Ran LiDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-7726-7569
Po-Lin LiuDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shu-Hang HeDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zi-Yin HanLeicester Medical School, University of Leicester, Leicester, UK.
Zhi-Han ShenDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0009-0006-1298-9006
Zhan-Ying WeiShanghai Clinical Research Centre of Bone Diseases, Department of Osteoporosis and Bone Diseases, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chang-Ru ZhangShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fei WangDepartment of Orthopaedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Helen DawesFaculty of Health and Life Science, Oxford Brookes University, Oxford, UK.ORCID https://orcid.org/0000-0002-2933-5213
Jian LuDepartment of Orthopaedic Surgery, Shanghai Eighth People's Hospital, Shanghai, China.ORCID https://orcid.org/0000-0002-2650-4990
Tong-He ZhuMultidisciplinary Innovation Centre for Bioadditive Manufacturing, Institute for Frontier Medical Technology, School of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai, China.ORCID https://orcid.org/0000-0002-7818-8168
Jin-Zhong ZhaoDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-2265-1878
Shang-Chun GuoDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shi-Cong TaoDepartment of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-8706-6138

Funding

National Natural Science Foundation of China 82072530National Natural Science Foundation of China 82372566National Natural Science Foundation of China 82472595Shanghai Jiao Tong University School of Medicine "Two-Hundred Talent" Program 2022-017Shanghai "Rising Stars of Medical Talent" Youth Development ProgramShanghai Sixth People's Hospital Excellent Young Scientist Development Program ynyq202101
6 · The paper itself

Abstract

Despite advances in bone tissue engineering, repairing diabetic bone defects remains a formidable challenge. Here, we present an innovative strategy for diabetic bone regeneration, the BCPG-MF@Y scaffold, which features diamond lattices of 3D-printed biphasic calcium phosphate (BCP) integrating porous gelatine methacryloyl (pGelMA) hydrogels embedded with Yoda1-functionalized manganese dioxide-ferritin (MF@Y) biomimetic nanozymes. Our comprehensive analyses revealed that the MF@Y nanozyme orchestrates mitochondrial homeostasis in bone mesenchymal stem cells (BMSCs), effectively scavenges mtROS, maintains mitochondrial membrane potential, modulates mitochondrial permeability transition pore dynamics, and prevents mitochondrial DNA leakage into the cytosol. This leads to inhibition of cGAS‒STING pathway activation, rejuvenation of senescent cells, reduced inflammation, and control of BMSC differentiation. Yoda1-mediated activation of Piezo1 mimics mechanical stimulation, promoting osteogenic differentiation while inhibiting adipogenic and osteoclastic differentiation. The BCPG-MF@Y scaffold synergistically reprograms the osteoimmune micromilieu by protecting mitochondria and activating Piezo1, showing significant promise for vascularized bone repair in diabetic conditions and potential applications in chronic inflammatory disorders.

Indexed as

3D‐printed diamond lattice scaffoldmitochondrial homeostasisnanozymevascularized bone repairYoda1

Identifiers

PMID42875724
PMCPMC13669222

What OpenQuestion 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 OpenQuestion graph.