Evidence map›Paper›PMID 38310454›Full record

SynthesisCurrent pharmaceutical biotechnology2024

Effects and Mechanisms of Fisetin against Ischemia-reperfusion Injuries: A Systematic Review.

Omid-Ali Adeli, Saeid Heidari-Soureshjani, Sahar Rostamian, Zahra Azadegan-Dehkordi, Armin Khaghani

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Current pharmaceutical biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. 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

5 authors at 4 institutions in 2 countries.

Omid-Ali AdeliDepartment of Pathology, Lorestan University of Medical Sciences, Khorramabad, Iran.ORCID 0000-0002-4183-4189
Saeid Heidari-SoureshjaniModeling in Health Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran.ORCID 0000-0002-7592-3868
Sahar RostamianDepartment of Medicine, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0003-4182-6004
Zahra Azadegan-DehkordiOriented Nursing Midwifery Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran.ORCID 0000-0003-1558-0645
Armin KhaghaniSkin Diseases and Leishmaniasis Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.ORCID 0000-0002-8145-7031
Shahrekord University of Medical Sciences · IRHarvard University · USIsfahan University of Medical Sciences · IRLorestan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemia-reperfusion injury (IRI) is a well-known ailment that can disturb organ function.

objectivesThis systematic review study investigated fisetin's effects and possible mechanisms in attenuating myocardial, cerebral, renal, and hepatic IRIs.

methodsThis systematic review included studies earlier than Sep 2023 by following the PRISMA statement 2020. After determining inclusion and exclusion criteria and related keywords, bibliographic databases, such as Cochrane Library, PubMed, Web of Science, Embase, and Scopus databases, were used to search the relevant studies. Studies were imported in End- Note X8, and the primary information was recorded in Excel.

resultsFisetin reduced reactive oxygen species (ROS) generation and upregulated antioxidant enzymes, such as superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and glutathione peroxidase (GPx), in ischemic tissues. Moreover, fisetin can attenuate oxidative stress by activating phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways. Fisetin has been indicated to prevent the activation of several pro-inflammatory signaling pathways, including NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) and MAPKs (Mitogen-activated protein kinases). It also inhibits the production of pro-inflammatory cytokines and enzymes like tumor necrosis factor-a (TNF-α), inducible-NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin-1β (IL-1β), IL-1, and IL-6. Fisetin attenuates IRI by improving mitochondrial function, anti-apoptotic effects, promoting autophagy, and preserving tissues from histological changes induced by IRIs.

conclusionFisetin, by antioxidant, anti-inflammatory, mitochondrial protection, promoting autophagy, and anti-apoptotic properties, can reduce cell injury due to myocardial, cerebral renal, and hepatic IRIs without any significant side effects.

Indexed as

FlavonolsOxidative StressReperfusion InjuryAnimalsAntioxidantsFlavonoidsHumansSignal TransductionAntioxidantsfisetinFlavonoidsFlavonolsCAT.cerebral ischemia-reperfusion injuryFisetinhepatic ischemia-reperfusion injurymyocardial ischemia-reperfusion injuryrenal ischemia-reperfusion injury

Identifiers

PMID38310454
OpenAlexW4391520144

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.