Aquaporin Membrane Channels in Oxidative Stress, Cell Signaling, and Aging: Recent Advances and Research Trends

Abstract

Reactive oxygen species (ROS) are produced as a result of aerobic metabolism and as by-products through numerous physiological and biochemical processes. While ROS-dependent modifications are fundamental in transducing intracellular signals controlling pleiotropic functions, imbalanced ROS can cause oxidative damage, eventually leading to many chronic diseases. Moreover, increased ROS and reduced nitric oxide (NO) bioavailability are main key factors in dysfunctions underlying aging, frailty, hypertension, and atherosclerosis. Extensive investigation aims to elucidate the beneficial effects of ROS and NO, providing novel insights into the current medical treatment of oxidative stress-related diseases of high epidemiological impact. This review focuses on emerging topics encompassing the functional involvement of aquaporin channel proteins (AQPs) and membrane transport systems, also allowing permeation of NO and hydrogen peroxide, a major ROS, in oxidative stress physiology and pathophysiology. The most recent advances regarding the modulation exerted by food phytocompounds with antioxidant action on AQPs are also reviewed.

Dehydration Sensitivity at the Early Seedling Establishment Stages of the European Beech (Fagus sylvatica L.)

“…In keeping with our results, increased amounts of electrolyte leakage were reported to be correlated with lowered viability in dehydrated seeds sensitive to desiccation [37,39,40] and contributed to formulating the cause-and-effect sequence, confirming experimentally that declined viability is driven by H 2 O 2 accumulation followed by elevated electrolyte leakage [37,40]. H 2 O 2 diffuses across cell membranes through the aquaporin channels [66] and spreads freely through disintegrated membranes in damaged tissue. Based on our previous studies of beech seed aging, the QC, an initial area of the apical meristem, was found to be a region accumulating ROS during seed storage and aging [14].…”

AQP1 modulates tendon stem/progenitor cells senescence during tendon aging

“…Here, we reported for the first time that AQP1 expression is closely correlated with TSPCs 26 . Altered expressions or functions of AQPs lead to fluid loss, and this loss is closely associated with cell aging 15 . Furthermore, AQPs can also facilitate the diffusion of reactive oxygen species, which lead to cellular alterations related to cell aging 15,27 .…”

“…Altered expressions or functions of AQPs lead to fluid loss, and this loss is closely associated with cell aging 15 . Furthermore, AQPs can also facilitate the diffusion of reactive oxygen species, which lead to cellular alterations related to cell aging 15,27 . Studies have showed that functional AQP1 is inserted into the plasma membrane 28,29 .…”

“…It has been extensively reported that AQPs are widely expressed in various tissues and associated with many physiological functions or diseases 13,14 . Fluid loss occurs in most tissues with age, and this loss is closely associated with altered expressions of AQPs 15 . Aquaporin 1 (AQP1) is one of the members of the AQPs family and has been reported to play a vital role in various biological and pathological events, such as proliferation, inflammation and migration 16 .…”

Cold Atmospheric Plasma: A Powerful Tool for Modern Medicine

“…The tumour cells also have more aquaporins [105] and this facilitates ROS and RNS penetration into the cell [106]. The degree of ROS and RNS diffusion into the cell can also be influenced by the membrane's lipid structure [107]. Cancer cells generally have lower levels of cholesterol and this makes cells more susceptible to peroxidation [108,109].…”