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Peer-reviewedCC BY-NC-NDTranslational pediatrics

MGST1 expression reduces ferroptosis of macrophage in pediatric asthma through tricarboxylic acid-mitochondrial damage by ALOX5 ubiquitination.

  • Caixia Lu1
  • Huan He1
  • Mingli Liu2
  1. 1Department of Pediatrics, Kongjiang Hospital, Shanghai, China.
  2. 2Department of Emergency, Kongjiang Hospital, Shanghai, China.
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Abstract

Pediatric asthma is a recurrent immune-mediated inflammatory airway disorder. This study aimed to investigate the functional role and underlying molecular mechanism of microsomal glutathione S-transferase 1 (MGST1) in the pathogenesis of pediatric asthma. An ovalbumin (OVA)-induced asthma mice model was established in vivo, and interleukin-4 (IL-4)-stimulated THP-1 cells were used to construct an in vitro inflammatory model. MGST1 messenger RNA (mRNA) expressions were significantly downregulated in lung tissues of asthmatic mice. Single-cell transcriptomic analysis further confirmed macrophage-specific enrichment of MGST1 in the asthmatic lung. Functional knockdown of MGST1 markedly exacerbated asthmatic inflammation in vivo. In contrast, MGST1 overexpression decreased the levels of immunoglobulin E (IgE) and IgG2a, suppressed the production of transforming growth factor beta (TGF-β) and IL-10, elevated interferon gamma (IFN-γ) expression, and reduced the levels of Th2/Th17-associated cytokines (IL-4, IL-5, and IL-17). Mechanistically, MGST1 alleviated macrophage oxidative stress, suppressed abnormal tricarboxylic acid cycle activation, and thereby attenuated mitochondrial damage and ferroptosis in asthmatic macrophages. Furthermore, MGST1 inhibited ALOX5 expression and directly interacted with the ALOX5 protein to facilitate its ubiquitination degradation. MGST1 suppresses macrophage ferroptosis in pediatric asthma by ALOX5 ubiquitination, which in turn inhibits tricarboxylic acid cycle dysfunction and mitochondrial injury. Accordingly, MGST1 represents a promising therapeutic target for pediatric asthma and other related pediatric inflammatory diseases.

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Cite

BibTeXRIS
BibTeX
@article{lu2026mgst1,
  title = {{MGST1 expression reduces ferroptosis of macrophage in pediatric asthma through tricarboxylic acid-mitochondrial damage by ALOX5 ubiquitination.}},
  author = {Caixia Lu and Huan He and Mingli Liu},
  journal = {Translational pediatrics},
  year = {2026},
  month = sep,
  doi = {10.21037/tp-2026-0341},
  url = {https://europepmc.org/article/MED/42996739},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - MGST1 expression reduces ferroptosis of macrophage in pediatric asthma through tricarboxylic acid-mitochondrial damage by ALOX5 ubiquitination.
AU  - Caixia Lu
AU  - Huan He
AU  - Mingli Liu
PY  - 2026
DA  - 2026/09/29
JO  - Translational pediatrics
DO  - 10.21037/tp-2026-0341
UR  - https://europepmc.org/article/MED/42996739
AB  - Pediatric asthma is a recurrent immune-mediated inflammatory airway disorder. This study aimed to investigate the functional role and underlying molecular mechanism of microsomal glutathione S-transferase 1 (MGST1) in the pathogenesis of pediatric asthma. An ovalbumin (OVA)-induced asthma mice model was established in vivo, and interleukin-4 (IL-4)-stimulated THP-1 cells were used to construct an in vitro inflammatory model. MGST1 messenger RNA (mRNA) expressions were significantly downregulated in lung tissues of asthmatic mice. Single-cell transcriptomic analysis further confirmed macrophage-specific enrichment of MGST1 in the asthmatic lung. Functional knockdown of MGST1 markedly exacerbated asthmatic inflammation in vivo. In contrast, MGST1 overexpression decreased the levels of immunoglobulin E (IgE) and IgG2a, suppressed the production of transforming growth factor beta (TGF-β) and IL-10, elevated interferon gamma (IFN-γ) expression, and reduced the levels of Th2/Th17-associated cytokines (IL-4, IL-5, and IL-17). Mechanistically, MGST1 alleviated macrophage oxidative stress, suppressed abnormal tricarboxylic acid cycle activation, and thereby attenuated mitochondrial damage and ferroptosis in asthmatic macrophages. Furthermore, MGST1 inhibited ALOX5 expression and directly interacted with the ALOX5 protein to facilitate its ubiquitination degradation. MGST1 suppresses macrophage ferroptosis in pediatric asthma by ALOX5 ubiquitination, which in turn inhibits tricarboxylic acid cycle dysfunction and mitochondrial injury. Accordingly, MGST1 represents a promising therapeutic target for pediatric asthma and other related pediatric inflammatory diseases.
SN  - 2224-4336
SN  - 2224-4344
ER  -