Evidence map›Paper›PMID 42862482›Full record

ReviewCardiovascular toxicology2026

Toxic Metals and Metalloids Exposure and the Gut-Cardiometabolic Axis: A Narrative Review of Microbiome Dysbiosis, Gut Barrier Dysfunction, and Metabolic Inflammation.

Ahmed Farid Gadelmawla, Sara Hosny El-Farargy, Amal A Alsubaiei, Najat Y AlSejari, Myriam Ramadan Sharara, Hamza A Abdul-Hafez, Ahmed Elmorsy Mohamed, Ahmed W Hageen, Abdullah M Alharran, Giuseppe Andò and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cardiovascular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Ahmed Farid GadelmawlaFaculty of Medicine, Menoufia University, Menoufia, Egypt. ahmedsaid140000@gmail.com.ORCID http://orcid.org/0000-0002-5802-2291
Sara Hosny El-FarargyFaculty of Medicine, Benha University, Benha, Egypt.
Amal A AlsubaieiKuwait Institute for Medical Specializations, Kuwait City, Kuwait.
Najat Y AlSejariKuwait Institute for Medical Specializations, Kuwait City, Kuwait.
Myriam Ramadan ShararaFaculty of Medicine, Misr University for Science and Technology, Giza, Egypt.
Hamza A Abdul-HafezDepartment of Medicine, Faculty of Medicine and Health Sciences, An- Najah National University, Nablus, Palestine. hamzaakrm12@gmail.com.
Ahmed Elmorsy MohamedDepartment of Internal Medicine, One Brooklyn Health Hospital, New York, USA.
Ahmed W HageenFaculty of Medicine, Tanta University, Tanta, Egypt.
Abdullah M AlharranCollege of Medicine and Medical Sciences, Arabian Gulf University, Manama, Kingdom of Bahrain.
Giuseppe AndòAzienda Ospedaliera Papardo, Messina, Italy.
Wilbert S AronowDepartments of Medicine and Cardiology, New York Medical College and Westchester Medical Center, New York, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toxic elements and metalloids exposure is an important environmental contributor to cardiometabolic disease, yet the gut-mediated mechanisms linking toxic elements to systemic metabolic and vascular injury remain incompletely understood. Lead, cadmium, arsenic, and mercury can enter the gastrointestinal tract through contaminated food, water, dust, smoking, seafood, and occupational sources, allowing direct interaction with the intestinal lumen, epithelial barrier, immune system, and gut microbiome. This narrative review examines the gut-cardiometabolic axis as a mechanistic framework connecting toxic metal exposure to microbiome dysbiosis, barrier dysfunction, endotoxemia, microbial metabolite imbalance, and chronic metabolic inflammation. Available evidence, derived from human, animal, and in-vitro studies of varying quality, suggests that toxic elements may alter microbial diversity and function, affect tight-junction integrity, and increase intestinal permeability; however, a consistent metal-specific signature and a complete causal chain have not been established. These changes may promote lipopolysaccharide passage through the intestinal barrier, activate innate immune pathways, and maintain systemic inflammatory signaling. At the same time, disruption of microbial metabolite profiles, including lower short-chain fatty acid production and altered trimethylamine N-oxide, bile acid and uremic toxin pathways, may promote insulin resistance, dyslipidemia, endothelial dysfunction, hypertension, atherosclerosis and overall cardiometabolic vulnerability. Viewing toxic-metal exposure through the gut-cardiometabolic axis provides a hypothesis-generating framework for integrating exposure reduction with conventional cardiometabolic risk management; the clinical value of microbiome-targeted strategies remains to be established. Longitudinal and multi-omics studies are still needed to define causal relationships and identify populations at greatest susceptibility.

Indexed as

BacteriaEnvironmental ExposureEnvironmental PollutantsGastrointestinal MicrobiomeInflammationInflammation MediatorsIntestinal Barrier FunctionIntestinesMetalloidsMetalsAnimalsCardiotoxicityDysbiosisHost-Pathogen InteractionsHumansRisk AssessmentEnvironmental PollutantsInflammation MediatorsMetalloidsMetalsGut microbiomeIntestinal barrierMetabolic endotoxemiaMicrobial metabolitesMicrobiome dysbiosisToxic metals and metalloids

Identifiers

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.