Evidence map›Paper›PMID 37118283›Full record

ArticleNature aging2022

Skin chronological aging drives age-related bone loss via secretion of cystatin-A.

Wenquan Liang, Qingjing Chen, Shasha Cheng, Ruiming Wei, Yuejun Li, Chenfeng Yao, Zhicong Ouyang, Dawei Kang, Ajuan Chen, Zezheng Liu and 4 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
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

37 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Development-based In Vivo Bioreactor Strategy for Challenging Senescent Bone Reconstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Galectin-9Aging cell · 2026
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  14. Article
  15. Integrative Aesthetics: Shaping the Emerging Frontier of Modern Aesthetic Medicine.Clinical, cosmetic and investigational dermatology · 2026
    Review
  16. Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Wenquan Liang *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0003-0881-6808
Qingjing Chen *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Shasha Cheng *Department of Clinical Laboratory, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Ruiming WeiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Yuejun LiDepartment of Orthopedics, The Second People's Hospital of Panyu District, Guangzhou, China.
Chenfeng YaoAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Zhicong OuyangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Dawei KangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Ajuan ChenAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Zezheng LiuAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Kai LiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Xiaochun BaiDepartment of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0001-9631-4781
Qingchu LiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Bin HuangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China. binxue483@163.com.ORCID http://orcid.org/0000-0001-6295-6647
Third Affiliated Hospital of Southern Medical University · CNPanyu Hospital of Chinese Medicine · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although clinical evidence has indicated an association between skin atrophy and bone loss during aging, their causal relationship and the underlying mechanisms are unknown. Here we show that premature skin aging drives bone loss in mice. We further identify that cystatin-A (Csta), a keratinocyte-enriched secreted factor, mediates the effect of skin on bone. Keratinocyte-derived Csta binds the receptor for activated C-kinase 1 in osteoblast and osteoclast progenitors, thus promoting their proliferation but inhibiting osteoclast differentiation. Csta secretion decreases with skin aging in both mice and humans, thereby causing senile osteoporosis by differentially decreasing the numbers of osteoblasts and osteoclasts. In contrast, topical application of calcipotriol stimulates Csta production in the epidermis and alleviates osteoporosis. These results reveal a mode of endocrine regulation of bone metabolism in the skin, and identify Csta as an epidermally derived hormone linking skin aging to age-related bone loss. Enhancers of skin Csta levels could serve as a potential topical drug for treatment of senile osteoporosis.

Indexed as

OsteoporosisSkin AgingAnimalsCystatin AHumansMiceOsteoblastsOsteoclastsCystatin A

Identifiers

PMID37118283
OpenAlexW4302363011

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.