Metabolic reprogramming on demand: enzymatic nanovesicles open a new frontier for acute kidney injury therapy
Peer-Reviewed Publication
Updates every hour. Last Updated: 6-Jun-2026 03:15 ET (6-Jun-2026 07:15 GMT/UTC)
Acute kidney injury (AKI) remains a life-threatening condition with high morbidity and mortality, yet no specific treatment is currently available. A key driver of AKI is the depletion of nicotinamide adenine dinucleotide (NAD+) in renal cells, which disrupts energy metabolism and leads to ATP deficiency and oxidative stress. The enzyme QPRT, essential for NAD+ synthesis, is markedly reduced during AKI—making it a promising but previously unexplored therapeutic target.
Now, researchers have developed a bioengineered enzymatic nanovesicle that restores NAD+ levels through dual mechanisms: delivering QPRT to boost NAD+ synthesis, while releasing olaparib to curb NAD+ consumption. This comprehensive metabolic reprogramming repairs mitochondria, enhances energy production, and reduces oxidative stress. The approach proved effective across multiple AKI models, including high‑dose chemotherapy‑induced kidney dysfunction, highlighting its potential as a safe and powerful therapeutic strategy.
Scientists from the National University of Singapore have successfully engineered a naturally occurring beneficial gut bacterium into a programmable “living medicine” to treat hepatic encephalopathy (HE), a severe brain dysfunction linked to liver failure. The therapy combines two engineered gut-bacteria strains: one absorbs excess gut ammonia and converts it into nutrients lacking in HE patients, while the other reduces ammonia production. Compared with a standard HE antibiotic, the cocktail achieved stronger improvements in anxiety and short-term memory, while also reduced inflammation in the brain.
Mothers provide a hidden immune legacy that protects their children's teeth long after weaning is over. A new study reveals how maternal antibodies act as early life architects, programming the mouth to resist aggressive bacteria and prevent the bone loss associated with adult gum disease. By setting a healthy immune tone before birth, these maternal defenses ensure that the foundation for a lifetime of oral health is laid from the very beginning.
The finding explains how the absence of a key protein in the structure of bile ducts promotes the onset of fibrosis.
If bile ducts let bile acids leak through, these will cause damage that liver tissue repairs by producing scars. The accumulation of these scars leads to fibrosis.
For the study’s authors, "this finding allows research to be steered towards safer therapies targeting liver fibrosis."
The paper is published in Nature Metabolism.
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