Evidence map›Paper›PMID 42899164›Full record

ArticleGenes & diseases2027

Betaine alleviates renal osteodystrophy by stabilizing ABCG1 mRNA to inhibit HMOX1-mediated ferroptosis in BMSCs.

Xinhang Li, Yi Xie, Wenyan Ren, Qing Liu, Qiming Pang, Wenting Liu, Xin Li, Bin He, Dongmei He, Xinyue Wan and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2027. 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
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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

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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

15 authors.

Xinhang LiDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yi XieDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Wenyan RenDepartment of Pharmacy, Beijing Anzhen Nanchong Hospital, Capital Medical University & Nanchong Central Hospital, Nanchong, Sichuan 637000, China.
Qing LiuDepartment of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Qiming PangDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Wenting LiuKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Xin LiKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Bin HeDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Dongmei HeKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Xinyue WanKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Jia LiuKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Jie CaiKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Baicheng HeKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Wei HuangDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Fang HeDepartments of Nephrology, Orthopedics, Urological Metabolism and Immunoecology Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal osteodystrophy is a debilitating complication of chronic kidney disease characterized by deteriorated bone microarchitecture and impaired bone formation, leading to increased fracture risk. Despite the pressing need for anabolic therapies, the cellular mechanisms by which uremic stress compromises osteoprogenitor function remain poorly defined. Here, metabolomic profiling of renal osteodystrophy patient cohorts revealed a profound depletion of circulating betaine. We show that betaine supplementation not only rescued the osteogenic differentiation of bone marrow-derived mesenchymal stem cells challenged with the uremic toxin indoxyl sulfate but also ameliorated skeletal deterioration in a rat model of chronic kidney disease. Mechanistically, we demonstrated that indoxyl sulfate triggered ferroptosis in bone marrow-derived mesenchymal stem cells-characterized by iron-dependent lipid peroxidation and aberrant HMOX1 up-regulation-thereby arresting osteogenesis. Betaine mitigates this ferroptotic stress through a novel post-transcriptional mechanism. Specifically, betaine down-regulated the RNA-binding protein hnRNP A1, preventing the recruitment of the CNOT1 deadenylase complex. This inhibition stabilized

Indexed as

ABCG1BetaineBone marrow mesenchymal stem cellsChronickidney diseaseChronic kidney disease–mineral and bone disorderFerroptosisRenal osteodystrophy

Identifiers

PMID42899164
PMCPMC13679308

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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.