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.

Organ and vessel-type-specific differences in endothelial cell barrier composition and properties uncover the distinct importance of the major tight junction protein Claudin5 in restricting agonist-induced leakage.

Acute hypoxia activates TRPA1 channels in cerebral artery endothelial cells to activate an early adaptive response to reduce tissue ischemic damage through vasodilation.

Inhibition of RyR2 hyperactivity with dantrolene not only prevents VT/VF and SCD but also heart failure by mitigating calcium dysfunction in pressure-overloaded hearts.

Local tissue hypoxia follows seizures, is responsible for postictal behavioural dysfunction rather than the seizures per se and can be treated.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.

To investigate why bats are long-lived and cancer-resistant, multi-omic data from bat and human cells was analyzed using computational flux modeling, suggesting dysregulation of succinate-fumarate dynamics and an ischemic-like basal metabolism in bat cells.

The combination of NSCs with NSC-derived exosomes ameliorated the injury of brain tissue including cerebral infarction, neuronal death, and glial scarring, and promoted the recovery of motor function.

Targeting mir128-3p could prevent cardiac insulin resistance in the non-infarcted myocardium and limit cardiac injury after myocardial infarction, delaying the development of heart failure.

It may be possible to treat cardiac hypertrophy and injury by using drugs that inhibit a protein called SIRT2.