Evidence map›Paper›PMID 35904600›Full record

ReviewCellular and molecular life sciences : CMLS2022

Metabolic reprogramming consequences of sepsis: adaptations and contradictions.

Jingjing Liu, Gaosheng Zhou, Xiaoting Wang, Dawei Liu

Open access · bronzeAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 3 pooled it
9.0field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 3 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. IL-18-associated basophil and mast cell activation in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. mRedox biology · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Observational
  17. Article
  18. Review
  19. Review
  20. Article

27 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Jingjing LiuDepartment of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, 1# Shuai Fu Yuan, Dong Cheng District, Beijing, 100730, China.
Gaosheng ZhouDepartment of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, 1# Shuai Fu Yuan, Dong Cheng District, Beijing, 100730, China.
Xiaoting WangDepartment of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, 1# Shuai Fu Yuan, Dong Cheng District, Beijing, 100730, China.
Dawei LiuDepartment of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, 1# Shuai Fu Yuan, Dong Cheng District, Beijing, 100730, China. daweiliu05@163.com.ORCID http://orcid.org/0000-0002-7728-1870
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Beijing Municipal Science and Technology Commission Z201100005520038
6 · The paper itself

Abstract

During sepsis, the importance of alterations in cell metabolism is underappreciated. The cellular metabolism, which has a variable metabolic profile in different cells and disease stages, is largely responsible for the immune imbalance and organ failure associated with sepsis. Metabolic reprogramming, in which glycolysis replaces OXPHOS as the main energy-producing pathway, is both a requirement for immune cell activation and a cause of immunosuppression. Meanwhile, the metabolites produced by OXPHOS and glycolysis can act as signaling molecules to control the immune response during sepsis. Sepsis-induced "energy shortage" leads to stagnated cell function and even organ dysfunction. Metabolic reprogramming can alleviate the energy crisis to some extent, enhance host tolerance to maintain cell survival functions, and ultimately increase the adaptation of cells during sepsis. However, a switch from glycolysis to OXPHOS is essential for restoring cell function. This review summarized the crosstalk between metabolic reprogramming and immune cell activity as well as organ function during sepsis, discussed the benefits and drawbacks of metabolic reprogramming to show the contradictions of metabolic reprogramming during sepsis, and assessed the feasibility of treating sepsis through targeted metabolism. Using metabolic reprogramming to achieve metabolic homeostasis could be a viable therapy option for sepsis.

Indexed as

Oxidative PhosphorylationSepsisGlycolysisHumansImmune ToleranceSignal TransductionGlycolysisImmunosuppressionMetabolic reprogrammingMODSOXPHOSSepsisTolerance

Identifiers

PMID35904600
PMCPMC9336160
OpenAlexW4288689653

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.