Aging of the carotid body

Abstract

The aging process is characterized by a decline in several physiological functions resulting in a reduced capability to maintain homeostasis. The lowered homeostatic capacity seems to involve the carotid body (CB), whose role is to modulate ventilation and tissue oxygen supply, thus playing a prime role in all aging processes. Aging causes marked changes in CB morphology. Indeed, it is enlarged and shows a concomitant decrease in the percentage of chemoreceptor tissue, as well as a proliferation of Type II cells. The carotid glomitis is present with aggregates of lymphocytes and fibrosis of the lobules. Type I cells are dehydrated, with a profound vacuolization, a shrinking nucleus, and lipofuscin accumulation. With increased age human CB shows a reduction in the number and volume of mitochondria, fewer synaptic junctions between glomi, along with a reduction in CB content of neurotransmitters, leading to a sort of 'physiological denervation'. Aging could be interpreted as a cumulative result of oxidative damage to cells, which derives from aerobic metabolism. Moreover, metabolism rate is tightly correlated with life duration, thus a loss in mitochondrial function is one of the prime factors affecting CB aging processes. The age-related reduction in synaptic junctions might be a self-protective mechanism through which cells buffer themselves against accumulation of reactive oxygen species. The correlation between hypoxia and life duration of CB cells remains open until the question of how and why cells sense oxygen is solved.

This article is protected by copyright. All rights reserved

from Physiology via xlomafota13 on Inoreader http://ift.tt/2FnKWpG
via IFTTT