Evidence map›Paper›PMID 34680089›Full record

ReviewBiomolecules2021

Metabolomic Studies for Metabolic Alterations Induced by Non-Steroidal Anti-Inflammatory Drugs: Mini Review.

Soumita Ghosh

Abstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Observational
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

1 author.

Soumita GhoshDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, Institute for Translational Medicine and Therapeutics, University of Pennsylvania, Philadelphia, PA 19104, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are Food and Drug Administration (FDA) approved antipyretic, anti-inflammatory, and analgesic drugs to mitigate pain, however it is associated with gastrointestinal injury and cardiovascular disease in some individuals. Metabolomics has the potential to understand the interaction of host and the drugs, such as NSAIDs administration. This discipline has been used by many researchers to understand the serious side effects of NSAIDs. We highlighted (1) the potential of metabolomics in understanding the pathogenesis of adverse events due to NSAIDs administration; (2) choice of metabolomics techniques, bio sample handling; (3) review of metabolomics studies in the front of NSAIDs in different biofluids and tissues; (4) pathway analysis of the data presented in the published literature. In our analysis we find tricarboxylic acid cycle (TCA), "glycine serine and threonine metabolism," "alanine, aspartate, and glutamate metabolism," and fatty acid metabolism to be altered by the NSAIDs like ibuprofen, indomethacin, naproxen, aspirin, and celecoxib. In conclusion, metabolomics allows the use of biological samples to identify useful pathways involved in disease progression, and subsequently inform a greater understanding of the disease pathogenesis. A further in-depth investigation of the associated pathways mentioned above holds the potential for drug targets for side effects mitigation.

Indexed as

MetabolomicsAnti-Inflammatory Agents, Non-SteroidalAspirinCelecoxibHumansIbuprofenInflammationMetabolomeAnti-Inflammatory Agents, Non-SteroidalAspirinCelecoxibIbuprofenmetabolomicsnon-steroidal anti-inflammatory drugspathway analysis

Identifiers

PMID34680089
PMCPMC8533408

What Socratic 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 Socratic graph.