Evidence map›Paper›PMID 34377234›Full record

ArticleAmerican journal of translational research2021

Knockdown of VDAC1 alleviates the cognitive dysfunction secondary to sepsis-associated encephalopathy.

Mengmeng Cai, Boxiang Du, Yanna Si, Juanjuan Miao, Jianyun Ge, Jiejie Zhang, Jie Song, Hongguang Bao

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. AQP4 Aggravates Cognitive Impairment in Sepsis-Associated Encephalopathy through Inhibiting NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  10. Review
  11. Review
  12. Article
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

8 authors at 2 institutions in 1 country.

Mengmeng CaiDepartment of Anesthesiology, Affiliated Nanjing Hospital of Nanjing Medical University (Nanjing First Hospital) Nanjing, Jiangsu Province, China.
Boxiang DuDepartment of Anesthesiology, The Second Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Yanna SiDepartment of Anesthesiology, Affiliated Nanjing Hospital of Nanjing Medical University (Nanjing First Hospital) Nanjing, Jiangsu Province, China.
Juanjuan MiaoDepartment of Anesthesiology, The Second Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Jianyun GeDepartment of Anesthesiology, The Second Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Jiejie ZhangDepartment of Anesthesiology, The Second Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Jie SongDepartment of Anesthesiology, The Second Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Hongguang BaoDepartment of Anesthesiology, Affiliated Nanjing Hospital of Nanjing Medical University (Nanjing First Hospital) Nanjing, Jiangsu Province, China.
Nantong University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-associated encephalopathy (SAE) is a serious and diffuse cerebral dysregulation with a high morbidity and mortality caused by sepsis. Mitophagy plays an important role in SAE, and microglial phagocytosis of apoptotic cells (efferocytosis) is the core of the brain regenerative response. Voltage dependent anion channel (VDAC1) is an important regulator of mitophagy. However, it remains unknown whether VDAC1 influences SAE progression by regulating mitophagy and efferocytosis. Herein, we explored the mechanism where knockdown of VDAC1 alleviated the cognitive dysfunction caused by sepsis-associated encephalopathy and further elucidated the underlying molecular mechanisms. SAE model in mice was established through caecal ligation and puncture (CLP). The increased mitophagy and decreased efferocytosis were observed by the transmission electron microscope (TEM) in the SAE model. Besides, immunoblot tests showed an interaction between autophagy and efferocytosis. Further behavior tests and TEM results indicated that knockdown of VDAC1 alleviated the cognitive dysfunction by decreasing the autophagy and increasing the efferocytosis in a PINK1/Parkin-dependent manner. Based on these results, we conclude that knockdown of VDAC1 alleviates the cognitive dysfunction in the CLP-induced SAE mouse model.

Indexed as

efferocytosismitophagyPINK1/Parkinsepsis-associated encephalopathyVDAC1

Identifiers

PMID34377234
PMCPMC8340252
OpenAlexW3188769932

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.