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Rooibos tea—in the cross fire of ROS, mitochondrial dysfunction and loss of proteostasis—positioned for healthy aging

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Abstract

Impaired mitochondrial function and loss of cellular proteostasis control are key hallmarks of aging and are implicated in the development of neurodegenerative diseases. A common denominator is the cell’s inability to handle reactive oxygen species (ROS), leading to major downstream oxidative damage that exacerbates neuronal dysfunction. Although we have progressed in understanding the molecular defects associated with neuronal aging, many unanswered questions remain. How much ROS is required to serve cellular function before it becomes detrimental and how does the cell’s oxidative status impact mitochondrial function and protein degradation through autophagy? How does ROS regulate autophagy? Aspalathus linearis, also commonly known as rooibos, is an endemic South African plant that is gaining globally acclaim for its antioxidant properties and its role as functional medicinal beverage. In this article we dissect the role of rooibos in the context of the cell’s ROS handling capacity, mitochondrial function and autophagy activity. By addressing the dynamic relationship between these critical interconnected systems, and by evaluating the functional properties of rooibos, we unravel its position for preserving cell viability and promoting healthy aging.

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Funding

The authors wish to acknowledge financial support from the South African Rooibos Council (SARC), Grant number 25062021.

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  1. Department of Physiological Sciences, Stellenbosch University, Merriman Avenue, Mike de Vries Building, Stellenbosch, 7600, South Africa

    Catherine Smit, Sholto De Wet, Tamryn Barron & Ben Loos

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  1. Catherine Smit
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CS and BL conceptualised and wrote the manuscript. CS prepared Figs. 1–3. All authors reviewed the manuscript.

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Correspondence to Ben Loos.

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Smit, C., De Wet, S., Barron, T. et al. Rooibos tea—in the cross fire of ROS, mitochondrial dysfunction and loss of proteostasis—positioned for healthy aging. Biogerontology 24, 149–162 (2023). https://doi.org/10.1007/s10522-022-10012-z

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