ReviewBiomedicines2021
The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.
Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 46 citations in OpenAlex.
- Zinc dyshomeostasis, mitochondrial dysfunction, and their pathological cycle in ischemic stroke pathophysiology: Mechanisms and potential therapeutic targets.Redox biology · 2026Review
- Mitochondrial degradation of metallothionein enables local zinc mobilization during zinc limitation.bioRxiv : the preprint server for biology · 2026Article
- Zinc Signaling in Acute Kidney Injury.Cells · 2026Review
- The zinc-nitric oxide axis in acute brain injury: Convergent oxidative-nitrative stress, peroxynitrite signaling, and therapeutic targets.Redox biology · 2026Review
- Zinc as a master regulator of intracellular organelle homeostasis.Experimental & molecular medicine · 2026Review
- Zinc-Mediated Lysosomal Destabilization Links Mitochondrial Damage to Neuronal Death in a Cellular MPPJournal of neurochemistry · 2026Article
- PRDM1-driven SLC30A9 overexpression contributes to the malignant phenotype of cervical cancer cells via promoting mitochondrial hyperfunction.Cell death & disease · 2025Article
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- A TRPM2-Driven Signalling Cycle Orchestrates Abnormal Inter-Organelle Crosstalk in Cardiovascular and Metabolic Diseases.Biomolecules · 2025Review
- Inter-Organelle Crosstalk in Oxidative Distress: A Unified TRPM2-NOX2 Mediated Vicious Cycle Involving CaAntioxidants (Basel, Switzerland) · 2025Review
- Pathways to the Brain: Impact of Fine Particulate Matter Components on the Central Nervous System.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- Revisiting Physicochemical and Biological Properties of ZnNanotechnology, science and applications · 2025Article
- Modulation of adipose inflammation and mitochondrial pathways by a yeast-derivedFrontiers in nutrition · 2025Article
- Research Progress on the Mechanisms of Protocatechuic Acid in the Treatment of Cognitive Impairment.Molecules (Basel, Switzerland) · 2024Review
- ZnBalkan medical journal · 2024Article
- Human platelets contain a pool of free zinc in dense granules.Research and practice in thrombosis and haemostasis · 2024Article
- Synaptic ZnNeurobiology of disease · 2024Article
- Evaluating Manganese, Zinc, and Copper Metal Toxicity on SH-SY5Y Cells in Establishing an Idiopathic Parkinson's Disease Model.International journal of molecular sciences · 2023Article
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
Abstract
Zinc is a highly abundant cation in the brain, essential for cellular functions, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential (MMP), leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and excitotoxic calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.
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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.