# Magnesium, Zinc and Copper in Lung Fibrosis: A Narrative Review

**Authors:** Mihai Nechifor, Carmen Lacramioara Zamfir, Cristina Gales

PMC · DOI: 10.3390/medicina62010010 · 2025-12-19

## TL;DR

This review explores how magnesium, zinc, and copper imbalances contribute to lung fibrosis and suggests their correction could improve treatment outcomes.

## Contribution

The paper highlights the novel role of magnesium, zinc, and copper imbalances in the pathogenesis of idiopathic pulmonary fibrosis and suggests early correction as a potential therapeutic strategy.

## Key findings

- Lower magnesium and zinc levels are commonly found in patients with idiopathic pulmonary fibrosis.
- Imbalances in these biometals are linked to key pathogenic mechanisms like oxidative stress and fibroblast proliferation.
- Correcting these imbalances early may enhance the effectiveness of existing treatments like pirfenidone and nintedanib.

## Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease with progressive evolution and high mortality. Magnesium, copper and zinc are essential biometals involved in numerous biological processes in all organs of the human body. A lower level of zinc and magnesium and a higher cooper/zinc ratio are frequently encountered in patients with idiopathic pulmonary fibrosis but also in other forms of pulmonary fibrosis. These imbalances are involved in the main pathogenic mechanisms of idiopathic pulmonary fibrosis: alveolar epithelial cell lesions, oxidative stress, inflammation, fibroblast and myofibroblast proliferation, mitochondrial activity, excessive extracellular matrix accumulation, high collagen production, alveolar macrophage dysfunctions, and apoptosis. A multitude of experimental and clinical studies have shown the importance of these bivalent cations for the synthesis or activity of some important endogenous active substances (fatty acids, eicosanoids, sirtuin1, p53 protein, interleukins, growth factors, some enzymes, and others) involved in one form or another in the pathogenesis of IPF. There are no randomized clinical trials yet, but some clinical and experimental results suggest that the association of zinc and magnesium with pirfenidone and nintedanib could be beneficial and should be assessed as soon as possible after the onset of this disease. The correction of hypomagnesemia and hypozincemia, whenever they exist, must be performed as soon as possible after the diagnosis of fibrosis.

## Linked entities

- **Chemicals:** magnesium (PubChem CID 5462224), zinc (PubChem CID 23994), copper (PubChem CID 23978), pirfenidone (PubChem CID 40632), nintedanib (PubChem CID 135423438)
- **Diseases:** idiopathic pulmonary fibrosis (MONDO:0800029)

## Full-text entities

- **Genes:** SIRT1 (sirtuin 1) [NCBI Gene 23411] {aka SIR2, SIR2L1, SIR2alpha}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}
- **Diseases:** lung disease (MESH:D008171), inflammation (MESH:D007249), IPF (MESH:D054990), hypomagnesemia (OMIM:613882), pulmonary fibrosis (MESH:D011658), Lung Fibrosis (MESH:D005355)
- **Chemicals:** pirfenidone (MESH:C093844), Copper (MESH:D003300), eicosanoids (MESH:D015777), nintedanib (MESH:C530716), fatty acids (MESH:D005227), Magnesium (MESH:D008274), Zinc (MESH:D015032)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12843507/full.md

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Source: https://tomesphere.com/paper/PMC12843507