ReviewThe FEBS journal2026
Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.
Review in The FEBS journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heavy metals like lead, cadmium, arsenic, mercury and chromium are persistent environmental contaminants recognised for their harmful effects on human health. Among their various toxicological effects, recent studies have identified endoplasmic reticulum (ER) as a critical target of HM-induced cellular damage. This review explores the contribution of HMs in disrupting ER homeostasis, with a particular focus on ER dysfunctions, ER stress mechanisms, calcium regulation, and ER-mitochondria crosstalk. ER stress occurs when its protein-folding capacity is exceeded, activating the unfolded protein response (UPR). Persistent ER stress, commonly induced by HM exposure, triggers apoptosis and contributes to several neurological diseases. A central aspect of HM-mediated ER dysfunctions involves the imbalance of ER Ca
Indexed as
Identifiers
What Socratic holds
Registered trials
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.