Aging and uremia: Is there cellular and molecular crossover?

Area of Science:

• Nephrology
• Gerontology
• Molecular Biology

Background:

• Chronic kidney disease (CKD) patients exhibit morphological and pathophysiological similarities to the geriatric population.
• Shared morbidity, mortality, and frailty profiles are noted, particularly in vascular and immune systems.
• Molecular and cellular similarities between aging and uremia require further investigation.

Purpose of the Study:

• To review and identify common molecular processes underlying aging and CKD.
• To explore shared cellular dysfunctions and their implications.
• To bridge the knowledge gap regarding molecular similarities between aging and uremia.

Main Methods:

• Literature review of published research on aging and CKD molecular pathways.
• Focused analysis on altered proteostasis, mitochondrial dysfunction, post-translational modification, and senescence.
• Examination of interrelated cell death and survival pathways (apoptosis, necroptosis, autophagy).

Main Results:

• Identified numerous common molecular characteristics between aging and CKD.
• Observed similar patterns of cellular dysfunction in both conditions.
• Highlighted the interconnectedness of apoptosis, necroptosis, and autophagy pathways.

Conclusions:

• Accelerated aging in CKD patients is rooted in shared molecular processes.
• Understanding these molecular underpinnings is crucial for developing novel therapies.
• Further research into these pathways could benefit patients with renal disease.