ArticleCellular and molecular life sciences : CMLS2016
Cadmium overkill: autophagy, apoptosis and necrosis signalling in endothelial cells exposed to cadmium.
Article in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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
30 citing papers in PubMed, 82 citations in OpenAlex.
- Empagliflozin Inhibits Cadmium-Induced Hepatic Cell Apoptosis Through Endoplasmic Reticulum Stress and Autophagy Pathways.Biological trace element research · 2025Article
- Mechanisms of ARA290 in counteracting cadmium-triggered neurotoxicity in PC12 cells.Toxicology research · 2025Article
- Essential and risk elements in horses affect haematology, serum biochemistry and oxidative status parameters.Scientific reports · 2025Article
- Acute Exposure to Cadmium Triggers NCOA4-Mediated Ferritinophagy and Ferroptosis in Never-Smokers Oral Cancer Cells.International journal of biological sciences · 2025Article
- Modulation of Angiotensin-II and Angiotensin 1-7 Levels Influences Cardiac Function in Myocardial Ischemia-reperfusion Injury.Current drug research reviews · 2025Review
- Effects of molecular interactions between the exposome and oxylipin metabolism on healthspan.Frontiers in physiology · 2025Review
- Dietary fiber intake moderates the impact of blood cadmium on depression: a nationally representative cross-sectional study.BMC public health · 2024Article
- Egg White Hydrolysate Mitigates Cadmium-induced Neurological Disorders and Oxidative Damage.Neurochemical research · 2024Article
- Review
- Associations between environmental heavy metals exposure and preserved ratio impaired spirometry in the U.S. adults.Environmental science and pollution research international · 2023Article
- Taurine Alleviates Cadmium-Induced Hepatotoxicity by Regulating Autophagy Flux.International journal of molecular sciences · 2023Article
- Article
- Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling.Experimental and therapeutic medicine · 2022Article
- Antitumor Activity and Physicochemical Properties of New Thiosemicarbazide Derivative and Its Co(II), Ni(II), Cu(II), Zn(II) and Cd(II) Complexes.Molecules (Basel, Switzerland) · 2022Article
- Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021Review
- Nano Selenium-Enriched Probiotics as Functional Food Products against Cadmium Liver Toxicity.Materials (Basel, Switzerland) · 2021Article
- Possible Role of Kaempferol in Reversing Oxidative Damage, Inflammation, and Apoptosis-Mediated Cortical Injury Following Cadmium Exposure.Neurotoxicity research · 2021Article
- Neuroinflammation and Microglial Activation at Rostral Ventrolateral Medulla Underpin Cadmium-Induced Cardiovascular Dysregulation in Rats.Journal of inflammation research · 2021Article
- Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic.Frontiers in pharmacology · 2021Review
- Effect of cell cycle synchronization on cadmium-induced apoptosis and necrosis in NRK-52E cells.Cell cycle (Georgetown, Tex.) · 2020Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis, necrosis, or autophagy-it is the mode of cell demise that defines the response of surrounding cells and organs. In case of one of the most toxic substances known to date, cadmium (Cd), and despite a large number of studies, the mode of cell death induced is still unclear. As there exists conflicting data as to which cell death mode is induced by Cd both across various cell types and within a single one, we chose to analyse Cd-induced cell death in primary human endothelial cells by investigating all possibilities that a cell faces in undergoing cell death. Our results indicate that Cd-induced death signalling starts with the causation of DNA damage and a cytosolic calcium flux. These two events lead to an apoptosis signalling-related mitochondrial membrane depolarisation and a classical DNA damage response. Simultaneously, autophagy signalling such as ER stress and phagosome formation is initiated. Importantly, we also observed lysosomal membrane permeabilization. It is the integration of all signals that results in DNA degradation and a disruption of the plasma membrane. Our data thus suggest that Cd causes the activation of multiple death signals in parallel. The genotype (for example, p53 positive or negative) as well as other factors may determine the initiation and rate of individual death signals. Differences in the signal mix and speed may explain the differing results recorded as to the Cd-induced mode of cell death thus far. In human endothelial cells it is the sum of most if not all of these signals that determine the mode of Cd-induced cell death: programmed necrosis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.