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Preclinical (animal model) · PMID 41934921

Elamipretide + H151 preserves alveolar-capillary architecture in experimental acute lung injury — VialBase Research

Elamipretide (ELM) improved redox status and reduced mitochondrial leak in LPS-induced ALI

Last updated · 2026 · Multiple authors · Tissue and Cell
Key findings
  • Elamipretide (ELM) improved redox status and reduced mitochondrial leak in LPS-induced ALI
  • ELM reduced cytosolic mtDNA and TFAM levels (mitochondrial danger signals)
  • H151 (STING inhibitor) suppressed interferon-chemokine induction
  • Combined ELM+H151 provided most comprehensive lung protection
  • Identifies mitochondrial danger-STING feed-forward axis as therapeutic target

PMID 41934921 — Elamipretide in Acute Lung Injury

Compound: SS-31 Citation: Tissue Cell. 2026 Mar 27:103514. doi:10.1016/j.tice.2026.103514

Summary

Investigated dual targeting of mitochondrial structure-function (elamipretide) and STING signaling (H151) in LPS-induced acute lung injury model.

Key Findings

  • Elamipretide effects: Improved redox status (reduced ROS, MDA; restored GSH, SOD), reduced mitochondrial leak (lower cytosolic mtDNA and TFAM)
  • H151 effects: Suppressed STING pathway (phospho-STING/TBK1/IRF3), reduced IFN-beta, IFN-alpha, CXCL10, CCL5
  • Combined ELM+H151: Greatest improvement in lung histology, reduced barrier disruption, inflammatory infiltration, and downstream signaling
  • Mechanistic insight: Mitochondrial damage releases mtDNA -> activates cGAS-STING -> amplifies inflammation. ELM breaks this cycle at the source.

Clinical Implications

Supports SS-31’s mechanism of preventing mitochondrial-driven inflammation. The combination approach (mitochondrial stabilization + downstream immune blockade) suggests SS-31 could complement anti-inflammatory therapies in acute and chronic inflammatory conditions.

PubMed

See Also

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