Harnessing plant thylakoids to restore cellular function in AKI

The kidney tubule is highly metabolically active and requires a constant supply of ATP for electrolyte and solute transport. Acute kidney injury (AKI) is associated with mitochondrial damage and metabolic disturbances, which impedes these processes. In particular, downregulation of quinolinate phosphoribosyltransferase (QPRT) leads to reduced levels of NAD⁺ — a key coenzyme for mitochondrial repair and ATP generation and a substrate for cellular antioxidant systems — that, in turn, lead to oxidative stress. Yao Lei and colleagues now demonstrate the ability of thylakoid-containing liposome vesicles to rescue AKI-associated energy deficits, increase ATP synthesis and suppress oxidative stress. “This work establishes a therapeutic paradigm for diseases characterized by compromised energy metabolism and dysregulated oxidative stress,” says lead author, Hai-Yan Xie.

Xie explains that her team has long drawn inspiration from native cellular components to construct bionic systems for biomedical applications. “When considering possible solutions for AKI treatment, we discovered that thylakoids — essential organelles for energy conversion in plant cells — possess a photosynthesis-driven electron transport chain and express abundant QPRT, which enables them to efficiently synthesize NAD⁺ and its derivatives such as NADH and NADPH,” she explains. “We hypothesized that thylakoids could be used to correct the metabolic dysfunction of AKI and reverse disease progression.”