Answers are grounded in this paper and cite their sources.
Inhibition of the PP5-5-LOX pathway or LTB4-BLT1 signaling may offer a therapeutic target to reduce maladaptive cardiac remodeling and fibrosis following myocardial infarction.
Arachidonic acid-driven LTB4 biosynthesis promotes macrophage and B-cell recruitment, contributing to sustaining inflammation and maladaptive cardiac tissue remodelling via the PP5–5-LOX pathway. Inhibition of PP5 or LTB4–BLT1 signalling reduces fibrosis, preserves cardiomyocytes, and enhances endothelial responses. BLT1, leukotriene B4 receptor 1; cPLA2, cytosolic phospholipase A2; CXCL13, chemokine (C-X-C motif) ligand 13; FLAP, 5-lipoxygenase-activating protein; KPNA1, karyopherin subunit alpha 1; LBT4, leukotriene B4; LOX, lipoxygenase; MI, myocardial infarction; PP5, protein phosphatase 5.
No takes yet. Share an insight, caveat, or question.
Marie‐Noëlle Giraud (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: