The Role of Metal Ions in Mitochondria: From Energy Metabolism to Cell Destiny.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic biology without original human or empirical data.
PubMed 42018027 · doi:10.1007/s12011-026-05112-7
What was done
This review integrates literature from metallomics and mitochondrial biology to summarize the biological roles of six metal ions—iron (Fe2+), copper (Cu+), sodium (Na+), calcium (Ca2+), zinc (Zn2+), and magnesium (Mg2+)—in mitochondrial energy metabolism, the electron transport chain, the tricarboxylic acid cycle, and cell fate regulation.
What was found
The abstract provides no empirical numbers or quantitative data. It describes mechanisms where disruption of metal ion homeostasis causes reactive oxygen species generation, loss of mitochondrial membrane potential, energy failure, and metal-dependent cell death forms including ferroptosis, copper-induced cell death, and sodium-dependent cell death.
Why it matters
It outlines how mitochondrial metal dysregulation contributes to cellular injury, providing a theoretical framework relevant to cancer, neurodegeneration, and cardiovascular disease therapeutics.
Limits
The work is a narrative review without primary clinical or experimental datasets, formal systematic review criteria, or quantitative effect sizes reported in the abstract.
Cited by
- supports The Krebs cycle in mitochondria requires magnesium as a cofactor at multiple enzymatic steps to generate ATP.