Evidence map›Paper›PMID 42961165›Full record

ArticleJournal of cellular and molecular medicine2026

Bazi Bushen Attenuates Skeletal Muscle Decline Associated With Oestrogen Deficiency and Modulates FGFR1/ERK Signalling.

Dezhi Huang, Na Xu, Qi Chu, Zhenhua Jia, Yan Wang, Jin Xu

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 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
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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

6 authors.

Dezhi HuangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID https://orcid.org/0009-0000-7617-0821
Na XuKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Qi ChuKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Zhenhua JiaState Key Laboratory for Innovation and Transformation of Luobing Theory, Hebei Yiling Hospital, Shijiazhuang, Hebei, China.ORCID https://orcid.org/0000-0001-5132-1099
Yan WangKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID https://orcid.org/0009-0000-6763-0611
Jin XuKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education; Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID https://orcid.org/0009-0005-6557-3859

Funding

National Key Research and Development Program of China 2021YFC2501700National Key Research and Development Program of China 2021YFC2501705National Key Research and Development Program of China 2023YFC3504305the Shandong Provincial Natural Science Foundation ZR2023QH350the Taishan Scholar Construction Project Special Funding TS201712092
6 · The paper itself

Abstract

Postmenopausal oestrogen deficiency is associated with skeletal muscle loss and functional decline, thereby increasing the risk of sarcopenia in women. Considering the safety risks linked to hormone replacement therapy (HRT), alternative strategies are needed to attenuate skeletal muscle decline after menopause. A total of 24 female C57BL/6J mice were randomly assigned to four groups (n = 6 per group): Sham-operated (SHAM), ovariectomized (OVX), OVX treated with estradiol valerate (OVX + E2) and OVX treated with Bazi Bushen (OVX + BZBS). Skeletal muscle mass and function were evaluated in four groups. RNA sequencing was applied to explore the molecular mechanisms and key signalling pathways underlying BZBS-induced muscle protection. We further examined the role of the FGFR1/ERK signalling pathway in mediating the effects of BZBS on myogenic differentiation in C2C12 myoblasts. The results showed that OVX mice had reduced grip strength and skeletal muscle mass, increased fat accumulation, reduced lean mass and impaired metabolic activity. These phenotypic alterations were accompanied by myofiber atrophy, increased collagen staining, endocrine perturbations and elevated expression of p16, p21, Atrogin-1 and MuRF1. BZBS ameliorated these abnormalities. RNA-seq suggested that FGF/MAPK signalling may be involved. In D-gal-treated C2C12 myoblasts, BZBS reduced Atrogin-1 and MuRF1 expression while restoring MYHC and MYOG expression. Mechanistically, BZBS suppressed FGFR1/ERK signalling activation and bFGF partially reversed the protective effects of BZBS. Taken together, these findings suggest that FGFR1/ERK signalling may contribute to the protective effects of BZBS. Our findings provide evidence for the beneficial effects of BZBS on skeletal muscle deterioration associated with oestrogen deficiency.

Indexed as

EstrogensMAP Kinase Signaling SystemMuscle, SkeletalPlant ExtractsReceptor, Fibroblast Growth Factor, Type 1AnimalsCell LineEstradiolFemaleMiceMice, Inbred C57BLMyoblastsOvariectomySignal TransductionEstradiolEstrogensFgfr1 protein, mousePlant ExtractsReceptor, Fibroblast Growth Factor, Type 1Bazi BushenFGFR1/ERK signallingoestrogen deficiencyskeletal muscle deterioration

Identifiers

PMID42961165
PMCPMC13721902

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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.