Acyl-CoA synthetase long-chain family member 4 (ACSL4)

Where the papers sit

10 papers from the last 6 months study Acyl-CoA synthetase long-chain family member 4 (ACSL4) directly · updated from PubMed 7 Oct 2026

• Therapeutic Ferroptosis Control

  ACSL4-mediated ferroptosis is being treated as a reversible driver of tissue injury and neuronal dysfunction. Parkin-dependent ubiquitination and brain-targeted PROTACs suppress ACSL4, while triacsin C and nanoparticle delivery extend lipid-metabolism interventions. ZDHHC9-mediated palmitoylation instead promotes ACSL4 activity in diabetes-related erectile dysfunction. The recurring goal is tissue protection through selective control of ACSL4 and lipid peroxidation.

  4 papers · 40%

• Ferroptosis in Tissue Injury

  Iron-driven reactive oxygen species and ferroptosis are emerging as shared mechanisms of kidney, heart, and brain injury. Polydopamine nanoparticles, ATP11B-YAP targeting, and mitochondrial protection all aim to suppress lipid peroxidation and restore cellular function. ACSL1-associated ischemia-reperfusion injury and ACSL4-related ferroptosis connect metabolic remodeling with tissue damage. The field is moving toward integrated biomarker discovery and targeted ferroptosis inhibitors, but therapeutic targets remain disease-specific.

  4 papers · 40%

• Ferroptosis and Lipid Peroxidation

  ACSL4-linked lipid peroxidation is being manipulated in both cancer therapy and vascular protection. Schisandrin B induces ferroptosis to restrain pancreatic cancer, whereas Salvianolic acid B activates NRF2-dependent defenses to preserve microvascular integrity. Ferrostatin-1, glutathione synthesis, and SLC3A2 recur as markers of the balance between injury and rescue. The work supports context-dependent ferroptosis control rather than one universal direction.

  2 papers · 20%