International journal of stem cellsOct 20, 2026

TAOK1 may protect older mice from kidney injury after blood flow returns by activating a cell cleanup process

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 21, 2026

Abstract

TAOK1 expression is significantly downregulated in the kidneys of aged mice.

Aged mice show increased susceptibility to acute kidney injury (AKI) following renal ischemia-reperfusion injury.
Overexpression of TAOK1 in aged mice improves renal function and reduces tubular damage, inflammation, and fibrosis.
TAOK1 appears to activate the STK3/BNIP3 signaling pathway, enhancing the process of removing damaged mitochondria (mitophagy).
Knockdown of TAOK1 in renal tubular cells from aged mice worsens cell injury and reduces mitophagy in response to hypoxia-reoxygenation.
The decline in TAOK1 with age may be linked to an increased risk of AKI, suggesting it could be a target for therapeutic interventions.

Simplified

The elderly suffer from a higher incidence and greater severity of acute kidney injury (AKI), yet the underlying molecular mechanisms remain poorly understood. This study dissects the possible role of thousand and one amino acid protein kinase 1 (TAOK1) in age-related AKI, specifically examining its regulation of mitophagy. Aged (23~24 months) C57BL/6 mice were subjected to renal ischemia-reperfusion injury (IRI) and TAOK1 was overexpressed in these mice. Renal function, histopathology, inflammation, neutrophil extracellular trap (NET) formation, and fibrosis were assessed. The involvement of the STK3/BNIP3 pathway and mitophagy was evaluated by Western blot and immunofluorescence. In vitro, primary renal tubular cells from aged mice underwent hypoxia-reoxygenation (H/R) following Taok1 knockdown. TAOK1 expression was significantly downregulated in the kidneys of aged mice. Taok1 overexpression in aged mice ameliorated IRI-induced renal dysfunction, tubular damage, inflammation, NET formation, and fibrosis. Mechanistically, Taok1 overexpression activated the STK3/BNIP3 signaling pathway and enhanced mitophagy, as evidenced by increased expressions of key mitophagy-related proteins. Conversely, Taok1 knockdown in aged mouse renal tubular cells exacerbated H/R-induced cell injury and apoptosis, and suppressed the STK3/BNIP3 pathway and mitophagy. Our findings demonstrate that TAOK1 protects against renal IRI in aged mice by promoting mitophagy through the STK3/BNIP3 axis. The age-related decline in TAOK1 may contribute to the heightened susceptibility to AKI, positioning TAOK1 as a potential therapeutic target for mitigating AKI in the aging population.

TAOK1 may protect older mice from kidney injury after blood flow returns by activating a cell cleanup process

Abstract

You found one interesting study. We’ll send the next 7.

What Lands in Your Inbox Each Week:

Recent issues from the longevity & aging brief