Evidence map›Paper›PMID 40618025›Full record

ArticleBMC cardiovascular disorders2025

Klotho modulation by tempol: a potential therapeutic axis in sepsis.

Alaa Al-Kadi, Aliaa F Anter, Remon Roshdy Rofaeil, Mohamed M Sayed-Ahmed, Sara Mohamed Naguib Abdel Hafez, Al-Shaimaa F Ahmed

Abstract read
In one paragraph

Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Alaa Al-KadiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Deraya University, Minia, Egypt.
Aliaa F AnterDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, Minia, Egypt.
Remon Roshdy RofaeilDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Deraya University, Minia, Egypt.
Mohamed M Sayed-AhmedPharmacology and Experimental Oncology Unit, National Cancer Institute, Cairo University, Cairo, Egypt.
Sara Mohamed Naguib Abdel HafezHistology and Cell Biology Department, Faculty of Medicine, Minia University, Minia, 6111, Egypt.
Al-Shaimaa F AhmedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, Minia, Egypt. Shaimaa.faissal@minia.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis is characterized by massive inflammatory and oxidative stress responses. The imbalance between oxidant and antioxidant activities during sepsis contributes to hyperinflammation, oxidation, endothelin system activation, and apoptosis, key elements of multiorgan failure. The current study investigated the role of tempol attenuating sepsis-induced acute cardiorenal injuries through modulation of Klotho.

methodWe used a cecal ligation and puncture (CLP) model of sepsis. Survival rate, histopathological assessment, and cardiorenal functions were analyzed. Oxidant and antioxidant activities, IL-6, and lactate were measured. The expression of tumor necrosis factor- α (TNF-α), p38-mitogen activating protein kinase (p38-MAPK), klotho, and caspase-3 were evaluated by immunohistochemistry.

resultsCLP caused acute cardiorenal damage, high mortality, upregulated levels of IL-6 and lactate, an imbalance in oxidant/antioxidant activities, elevated expression of TNF-α, p38, caspase-3, and reduced expression of klotho. Tempol improved survival, reduced inflammatory and oxidative stress parameters, improved cardiorenal functions, elevated the tissue contents of reduced glutathione (GSH) and superoxide dismutase (SOD), raised the expression of klotho protein and reduced the expression of p38, TNF- α and caspase-3.

conclusionTempol is a promising agent against sepsis-induced organ damage. This was evident in its cardiorenal protective effect, up-regulation of klotho, suppression of inflammation, oxidation, and apoptosis, and enhancement of the antioxidant status.

Indexed as

Acute Kidney InjuryAnti-Inflammatory AgentsAntioxidantsCyclic N-OxidesGlucuronidaseKidneyOxidative StressSepsisAnimalsApoptosisCaspase 3Disease Models, AnimalGlutathioneInflammation MediatorsInterleukin-6Klotho ProteinsAnti-Inflammatory AgentsAntioxidantsCasp3 protein, mouseCasp3 protein, ratCaspase 3Cyclic N-OxidesGlucuronidaseGlutathioneInflammation MediatorsInterleukin-6Klotho ProteinsLactic Acidp38 Mitogen-Activated Protein KinasesSpin LabelstempolTumor Necrosis Factor-alphaHeartKidneyKlothoOxidationSepsisTempol

Identifiers

PMID40618025
PMCPMC12229035

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Registered trials

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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.