Molecular aspects of renal senescence
Roland Schmitt1, Nathan Susnik, Anette Melk
1aDepartment of Nephrology and Hypertension, Hannover Medical School bDepartment of Kidney, Liver and Metabolic Diseases, Children's Hospital, Hannover Medical School, Hannover, Germany.
Purpose Of Review:
The aging kidney undergoes profound changes that lead to a reduction in stress resistance and impaired repair capacity. In order to improve the outcome of acute and chronic kidney damage, it is instrumental to understand the mechanisms that cause these changes. Cellular senescence has emerged as an important cellular process that contributes to age-associated kidney changes and chronic kidney disease progression.
Recent Findings:
New mechanistic insights into excessive intracellular glucose, advanced glycation end products and endoplasmatic reticulum stress further support the importance of cellular senescence in the development of diabetic nephropathy. As telomere length of leukocytic DNA is increasingly used as a biomarker to estimate senescence in clinical cohort studies, this review also summarizes the literature on telomere length with respect to the kidney and evaluates the strengths and weaknesses of this methodology. Furthermore, novel findings on the relationships among telomeres, senescence and autophagy are discussed.
Summary:
Cellular senescence contributes to the decline in renal function during aging and defective regeneration in kidney diseases. Further insight into the underlying molecular mechanisms of senescence will establish a basis for preventive strategies that improve renal stress resistance and regenerative capacity.
Insights
Cellular senescence drives kidney aging and disease progression by impairing repair. Understanding senescence mechanisms is key to improving kidney stress resistance and regeneration for better outcomes.
Area of Science:
- Nephrology
- Gerontology
- Cellular Biology
Background:
- Aging kidneys exhibit reduced stress resistance and impaired repair capacity.
- Cellular senescence is a key process in age-associated kidney changes and chronic kidney disease (CKD) progression.
- Understanding senescence mechanisms is crucial for improving outcomes in acute and chronic kidney damage.
Purpose of the Study:
- To review the role of cellular senescence in kidney aging and disease.
- To explore mechanistic insights into senescence in diabetic nephropathy.
- To evaluate telomere length as a biomarker for senescence in kidney studies.
Main Methods:
- Literature review of cellular senescence in kidney aging and disease.
- Analysis of mechanistic insights into hyperglycemia, advanced glycation end products, and endoplasmic reticulum stress.
- Evaluation of studies on telomere length as a biomarker for senescence in kidney disease.
Main Results:
- Cellular senescence contributes to declining renal function in aging and defective regeneration in kidney diseases.
- Excessive intracellular glucose, advanced glycation end products, and ER stress highlight senescence's role in diabetic nephropathy.
- Telomere length is explored as a biomarker, with its strengths and weaknesses discussed in relation to kidney senescence and autophagy.
Conclusions:
- Cellular senescence is a significant factor in age-related kidney decline and impaired regeneration.
- Further research into senescence mechanisms will enable strategies to enhance renal stress resistance and repair.
- Targeting cellular senescence may offer therapeutic avenues for improving kidney health in aging and disease.
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