Evidence map›Paper›PMID 37223476›Full record

ArticleResearch (Washington, D.C.)2023

Unresolved Excess Accumulation of Myelin-Derived Cholesterol Contributes to Scar Formation after Spinal Cord Injury.

Bolin Zheng, Yijing He, Shuai Yin, Xu Zhu, Qing Zhao, Huiyi Yang, Zhaojie Wang, Rongrong Zhu, Liming Cheng

Open access · goldAbstract read
In one paragraph

Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 18 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Bolin ZhengKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Yijing HeKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Shuai YinKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Xu ZhuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Qing ZhaoKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Huiyi YangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Zhaojie WangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Rongrong ZhuKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Liming ChengKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration, Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal cord injury triggers complex pathological cascades, resulting in destructive tissue damage and incomplete tissue repair. Scar formation is generally considered a barrier for regeneration in the central nervous system. However, the intrinsic mechanism of scar formation after spinal cord injury has not been fully elucidated. Here, we report that excess cholesterol accumulates in phagocytes and is inefficiently removed from spinal cord lesions in young adult mice. Interestingly, we observed that excessive cholesterol also accumulates in injured peripheral nerves but is subsequently removed by reverse cholesterol transport. Meanwhile, preventing reverse cholesterol transport leads to macrophage accumulation and fibrosis in injured peripheral nerves. Furthermore, the neonatal mouse spinal cord lesions are devoid of myelin-derived lipids and can heal without excess cholesterol accumulation. We found that transplantation of myelin into neonatal lesions disrupts healing with excessive cholesterol accumulation, persistent macrophage activation, and fibrosis. Myelin internalization suppresses macrophage apoptosis mediated by CD5L expression, indicating that myelin-derived cholesterol plays a critical role in impaired wound healing. Taken together, our data suggest that the central nervous system lacks an efficient approach for cholesterol clearance, resulting in excessive accumulation of myelin-derived cholesterol, thereby inducing scar formation after injury.

Identifiers

PMID37223476
PMCPMC10202378
OpenAlexW4366122391

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.