Evidence map›Paper›PMID 35618183›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2022

Hormone sensitive lipase ablation promotes bone regeneration.

Wen-Jun Shen, Chris Still Ii, Lina Han, Pinglin Yang, Jia Chen, Michael Wosczyna, Benjamin Jean Rene Salmon, Kristy C Perez, Jingtao Li, Pedro L Cuevas and 5 more

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 56% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Wen-Jun ShenDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Chris Still IiInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA, USA.
Lina HanDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Pinglin YangDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Jia ChenDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Michael WosczynaDepartment of Neurology and Neurological Sciences, Stanford School of Medicine, Stanford, CA, USA.
Benjamin Jean Rene SalmonDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Kristy C PerezDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Jingtao LiDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Pedro L CuevasDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Bo LiuDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Salman AzharDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Jill HelmsDivision of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA.
Lei S QiDepartment of Bioengineering, Stanford University, Stanford, CA, USA; Sarafan ChEM-H, Stanford University, Stanford, CA, USA; Chan Zuckerberg Biohub, San Francisco, Stanford, CA, USA. Electronic address: slqi@stanford.edu.
Fredric B KraemerDivision of Endocrinology, Gerontology, and Metabolism, Stanford University, Stanford, CA, USA; Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA; Stanford Diabetes Research Center, Stanford, CA, USA. Electronic address: fbk@stanford.edu.
Stanford Medicine · USVA Palo Alto Health Care System · USCalifornia Institute for Regenerative Medicine · USChan Zuckerberg Initiative (United States) · US

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
BLRD VA I01 BX000398BLRD VA I01 BX001923BLRD VA IK6 BX004200NIDDK NIH HHS P30 DK116074
6 · The paper itself

Abstract

There is an inverse relationship between the differentiation of mesenchymal stem cells (MSCs) along either an adipocyte or osteoblast lineage, with lineage differentiation known to be mediated by transcription factors PPARγ and Runx2, respectively. Endogenous ligands for PPARγ are generated during the hydrolysis of triacylglycerols to fatty acids through the actions of lipases such as hormone sensitive lipase (HSL). To examine whether reduced production of endogenous PPARγ ligands would influence bone regeneration, we examined the effects of HSL knockout on fracture repair in mice using a tibial mono-cortical defect as a model. We found an improved rate of fracture repair in HSL-ko mice documented by serial μCT and bone histomorphometry compared to wild-type (WT) mice. Similarly, accelerated rates of bone regeneration were observed with a calvarial model where implantation of bone grafts from HSL-ko mice accelerated bone regeneration at the injury site. Further analysis revealed improved MSC differentiation down osteoblast and chondrocyte lineage with inhibition of HSL. MSC recruitment to the injury site was greater in HSL-ko mice than WT. Finally, we used single cell RNAseq to understand the osteoimmunological differences between WT and HSL-ko mice and found changes in the pre-osteoclast population. Our study shows HSL-ko mice as an interesting model to study improvements to bone injury repair. Furthermore, our study highlights the potential importance of pre-osteoclasts and osteoclasts in bone repair.

Indexed as

PPAR gammaSterol EsteraseAnimalsBone RegenerationLigandsMiceMice, KnockoutLigandsPPAR gammaSterol EsteraseBone repairHormone sensitive lipaseKnockout mice

Identifiers

PMID35618183
PMCPMC12834040
OpenAlexW4281400104

What OpenQuestion holds

Textmetadata
LicenceTDM
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.