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Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning
Stanislovas S Jankauskas1, Denis N Silachev1,2, Nadezda V Andrianova1,3
1a A.N. Belozersky Institute of Physico-Chemical Biology , M.V. Lomonosov Moscow State University , Moscow , Russian Federation.
Abstract:
The anti-aging strategy is one of the main challenges of the modern biomedical science. The term "aging" covers organisms, cells, cellular organelles and their constituents. In general term, aging system admits the existence of nonfunctional structures which by some reasons have not been removed by a clearing system, e.g., through autophagy/mitophagy marking and destroying unwanted cells or mitochondria. This directly relates to the old kidney which normal functioning is critical for the viability of the organism. One of the main problems in biomedical studies is that in their majority, young organisms serve as a standard with further extrapolation on the aged system. However, some protective systems, which demonstrate their efficiency in young systems, lose their beneficial effect in aged organisms. It is true for ischemic preconditioning of the kidney, which is almost useless for an old kidney. The pharmacological intervention could correct the defects of the senile system provided that the complete understanding of all elements involved in aging will be achieved. We discuss critical elements which determine the difference between young and old phenotypes and give directions to prevent or cure lesions occurring in aged organs including kidney.
Abbreviations:
AKI: acute kidney injury; I/R: ischemia/reperfusion; CR: caloric restriction; ROS: reactive oxygen species; RC: respiratory chain.
Insights
Aging affects kidneys, reducing protective mechanisms like ischemic preconditioning. Understanding age-related cellular changes is key to developing interventions for aged organ protection and treatment.
Area of Science:
- Biomedical science
- Gerontology
- Nephrology
Background:
- Aging impacts organisms, cells, and organelles, leading to accumulation of non-functional structures.
- Kidney function is vital, and aging impairs its protective systems, unlike in younger organisms.
- Current research often uses young organisms as a standard, limiting understanding of aged systems.
Purpose of the Study:
- To identify critical elements differentiating young and old phenotypes.
- To explore strategies for preventing or treating age-related kidney damage.
- To address the limitations of extrapolating findings from young to aged systems.
Main Methods:
- Review and discussion of age-related cellular and organ changes.
- Analysis of protective mechanisms in young versus aged kidneys.
- Exploration of potential pharmacological interventions for senile systems.
Main Results:
- Protective systems effective in young organisms may fail in aged ones, e.g., ischemic preconditioning in old kidneys.
- Accumulation of non-functional cellular components is a hallmark of aging.
- Differences between young and old phenotypes require specific understanding for therapeutic development.
Conclusions:
- A comprehensive understanding of aging mechanisms is necessary for effective pharmacological interventions.
- Targeting age-specific defects can potentially prevent or cure lesions in aged organs, including the kidney.
- Future research should focus on age-related differences rather than solely on young organism models.
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