Gut microbiota-derived gamma-aminobutyric acid is identified as a key metabolite that metformin protect from hepatic ischemia/reperfusion injury.

An unbiased approach unveils a non-canonical substrate of the known transporters, highlighting the mechanism behind the use of D-serine as a kidney biomarker.

Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.

The UPOAO model effectively replicates retinal ischemia in retinal artery occlusion, providing a novel platform for identifying pathogenic genes and advancing therapeutic research.

Renal capillary pericytes are a novel therapeutic target for reducing sustained reduction in renal blood flow ('no-reflow') after kidney ischaemia.

Myoglobin iron contributes to the formation and poor healing of muscle pressure injuries, that is, bedsores, and iron-chelation therapy can be administered after prolonged pressure to increase survival of the damaged tissue.

Ferroptotic stress enhances the accumulation of damage-associated inflammatory proximal tubular cell state, thereby promoting maladaptive renal repair and the AKI-to-CKD transition.

Immature CD10^neg neutrophils and CD14⁺HLA-DR^neg/low monocytes inducing proinflammatory and adaptive immune responses emerge in patients with large acute myocardial infarction.

Engineered mesenchymal stem cells (MSCs) could produce mutant β-galactosidase and trigger nitric oxide (NO) release when the NO prodrug is systemically administered, which can achieve NO release in a precise spatiotemporal manner and augment the therapeutic efficiency of MSCs.

Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.