Evidence map›Paper›PMID 40372601›Full record

ArticleBiological trace element research2025

Empagliflozin Inhibits Cadmium-Induced Hepatic Cell Apoptosis Through Endoplasmic Reticulum Stress and Autophagy Pathways.

Naeem F Qusty, Bayan T Bokhari, Medhat Taha, Mohammad Ahmad Alobaidy, Abdullah G Al-Kushi, Hatem A Sembawa, Omer Abdelbagi, Tourki A S Baokbah, Rami Obaid, Halah Tariq Albar and 2 more

Abstract read
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In one paragraph

Article in Biological trace element research, 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. 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

12 authors.

Naeem F QustyDepartment of Clinical Laboratory Sciences, Faculty of Applied Medical Sciences, Umm Al‒Qura University, Makkah, 21955, Saudi Arabia.
Bayan T BokhariDepartment of Clinical Laboratory Sciences, Faculty of Applied Medical Sciences, Umm Al‒Qura University, Makkah, 21955, Saudi Arabia.
Medhat TahaDepartment of Anatomy, Al-Qunfudah Medical College, Umm Al-Qura University, Al-Qunfudhah, Saudi Arabia. Medhattaha53@yahoo.com.
Mohammad Ahmad AlobaidyDepartment of Anatomy, Faculty of Medicine, Umm Al-Qura University, Makkah, P.O. Box 7607, Saudi Arabia.
Abdullah G Al-KushiDepartment of Anatomy, Faculty of Medicine, Umm Al-Qura University, Makkah, P.O. Box 7607, Saudi Arabia.
Hatem A SembawaDepartment of Surgery, Faculty of Medicine, Umm Al-Qura University, Holy Makkah, Saudi Arabia.
Omer AbdelbagiDepartment of Pathology, Qunfudah Faculty of Medicine, Umm-Al-Qura University, Makkah, Kingdom of Saudi Arabia.
Tourki A S BaokbahDepartment of Medical Emergency Services, College of Health Sciences-AlQunfudah, Umm Al-Qura University, Makkah, Saudi Arabia.
Rami ObaidDepartment of Medical Genetics, Faculty of Medicine, -Qunfudah, Umm Al-Qura University, Al-Qunfudhah, Saudi Arabia.
Halah Tariq AlbarDepartment of Physiology, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Omar BabateenDepartment of Physiology, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Naief DahranDepartment of Basic Medical Sciences, College of Medicine, University of Jeddah, Jeddah, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd), a well-known toxic heavy metal, adversely affects multiple organs. The SGLT-2 inhibitor empagliflozin (EMPA) exhibits significant antioxidant properties and hypoglycemic potential. This study aimed to investigate the hepatoprotective effect of EMPA against Cd-induced liver injury and elucidate its molecular mechanisms. Thirty-two male rats were allocated into four groups of eight rats each: group I (control group), group II (EMPA group), group III (Cd group), and group IV (Cd + EMPA group). Cd intake disrupted liver enzymes (ALT, AST, and ALP) and impaired hepatic histological architecture. Cd induced hepatic oxidative stress, as evidenced by increased MDA levels and reduced antioxidant enzymes, including SOD, GPx, and CAT. It downregulated the Nrf2/HO-1 pathway and elevated proinflammatory mediators IL-1β, IL-6, and TNF-α. Furthermore, Cd increased ER stress markers GRP78 and CHOP, along with apoptotic markers Bax and caspase-3 while decreasing anti-apoptotic Bcl-2 and reducing the autophagic indicator Beclin-1. Interestingly, EMPA administration in the Cd + EMPA group attenuated Cd-induced hepatic deterioration, improving hepatocyte structure. This beneficial effect was driven by the downregulation of hepatic oxidative stress, inflammation, ER stress, and apoptosis, alongside the upregulation of the autophagy process. In conclusion, this study highlights the hepatoprotective effect of EMPA against Cd-induced liver injury, elucidating its underlying molecular mechanisms.

Indexed as

ApoptosisAutophagyBenzhydryl CompoundsCadmiumEndoplasmic Reticulum StressGlucosidesHepatocytesSodium-Glucose Transporter 2 InhibitorsAnimalsLiverMaleOxidative StressRatsBenzhydryl CompoundsCadmiumempagliflozinGlucosidesSodium-Glucose Transporter 2 InhibitorsApoptosisAutophagyCadmiumEmpagliflozinEndoplasmic reticulum stressInflammationOxidative stress

Identifiers

PMID40372601

What OpenQuestion holds

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Read underepoch 390

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.