Evidence map›Paper›PMID 35562986›Full record

ReviewInternational journal of molecular sciences2022

Inflammation: A New Look at an Old Problem.

Evgenii Gusev, Yulia Zhuravleva

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
8.1field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Curcumin analogues suppress cellular pro-inflammatory mediators and reduce edema.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Evgenii GusevInstitute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, 620049 Ekaterinburg, Russia.ORCID 0000-0002-7145-2376
Yulia ZhuravlevaInstitute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, 620049 Ekaterinburg, Russia.ORCID 0000-0003-3266-0954
Institute of Immunology and Physiology · RU

Funding

The Government contract of the Institute of Immunology and Physiology 122020900136-4
6 · The paper itself

Abstract

Pro-inflammatory stress is inherent in any cells that are subject to damage or threat of damage. It is defined by a number of universal components, including oxidative stress, cellular response to DNA damage, unfolded protein response to mitochondrial and endoplasmic reticulum stress, changes in autophagy, inflammasome formation, non-coding RNA response, formation of an inducible network of signaling pathways, and epigenetic changes. The presence of an inducible receptor and secretory phenotype in many cells is the cause of tissue pro-inflammatory stress. The key phenomenon determining the occurrence of a classical inflammatory focus is the microvascular inflammatory response (exudation, leukocyte migration to the alteration zone). This same reaction at the systemic level leads to the development of life-critical systemic inflammation. From this standpoint, we can characterize the common mechanisms of pathologies that differ in their clinical appearance. The division of inflammation into alternative variants has deep evolutionary roots. Evolutionary aspects of inflammation are also described in the review. The aim of the review is to provide theoretical arguments for the need for an up-to-date theory of the relationship between key human pathological processes based on the integrative role of the molecular mechanisms of cellular and tissue pro-inflammatory stress.

Indexed as

Endoplasmic Reticulum StressInflammationAutophagyHumansOxidative StressUnfolded Protein Responseatherosclerosiscellular stressevolution of inflammationgeneral pathological processinflammationneurodegenerationsystemic inflammationtissue stresstumors

Identifiers

PMID35562986
PMCPMC9100490
OpenAlexW4224234386

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.