Involvement of nitric oxide and caveolins in the age-associated functional and structural changes in a heart under osmotic stress

Arza, Patricia; Netti, Vanina Alejandra; Perosi, Francisco; Cernadas, Gustavo; Ochoa, Federico; Magnani, Natalia; Evelson, Pablo; Zotta, Elsa; Fellet, Andrea L.; Balaszczuk, Ana M.

doi:10.1016/j.biopha.2014.12.026

Cited by 4 publications

(2 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, aging caused functional alterations in the cardiovascular system, evidenced by more remarkable ventricular NOS formation following water restriction and hypovolemia in adult rats. These findings demonstrate the roles of NO and its caveolin regulatory proteins in preserving cardiac physiological function during dehydration and aging [88].…”

Section: Cardiovascular Aging and Nomentioning

confidence: 55%

“…NO contributes to the regulation of water and electrolyte homeostasis in the cardiovascular system [87]. Arza et al (2015) found that, following 1-month water restriction, both young and adult rats showed decreased NOS expression and activity related to the increased caveolin-1 levels. Interestingly, aging caused functional alterations in the cardiovascular system, evidenced by more remarkable ventricular NOS formation following water restriction and hypovolemia in adult rats.…”

Section: Cardiovascular Aging and Nomentioning

confidence: 99%

See 1 more Smart Citation

An Overview of NO Signaling Pathways in Aging

et al. 2021

View full text Add to dashboard Cite

Nitric Oxide (NO) is a potent signaling molecule involved in the regulation of various cellular mechanisms and pathways under normal and pathological conditions. NO production, its effects, and its efficacy, are extremely sensitive to aging-related changes in the cells. Herein, we review the mechanisms of NO signaling in the cardiovascular system, central nervous system (CNS), reproduction system, as well as its effects on skin, kidneys, thyroid, muscles, and on the immune system during aging. The aging-related decline in NO levels and bioavailability is also discussed in this review. The decreased NO production by endothelial nitric oxide synthase (eNOS) was revealed in the aged cardiovascular system. In the CNS, the decline of the neuronal (n)NOS production of NO was related to the impairment of memory, sleep, and cognition. NO played an important role in the aging of oocytes and aged-induced erectile dysfunction. Aging downregulated NO signaling pathways in endothelial cells resulting in skin, kidney, thyroid, and muscle disorders. Putative therapeutic agents (natural/synthetic) affecting NO signaling mechanisms in the aging process are discussed in the present study. In summary, all of the studies reviewed demonstrate that NO plays a crucial role in the cellular aging processes.

show abstract

Section: Cardiovascular Aging and Nomentioning

confidence: 55%

Section: Cardiovascular Aging and Nomentioning

confidence: 99%

An Overview of NO Signaling Pathways in Aging

et al. 2021

View full text Add to dashboard Cite

show abstract

Role of tissue transglutaminase in age-associated ventricular stiffness

Pau

Steppan

et al. 2016

Amino Acids

View full text Add to dashboard Cite

Aging is associated with increased cardiomyocyte loss, left-ventricular hypertrophy, and the accumulation of extracellular matrix, which results in declining cardiac function. The role of the matrix crosslinking enzyme, tissue transglutaminase (TG2), in age-related myocardial stiffness, and contractile function remains incompletely understood. In this study, we examined the role of TG2 in cardiac function, and determined whether TG2 inhibition can prevent age-associated changes in cardiac function. Male Fisher rats (18-month-old) were administered the transglutaminase inhibitor cystamine (study group) or saline (age-matched controls) for 12 weeks via osmotic mini-pumps. Cardiac function was determined by echocardiography and invasive pressure-volume loops. Rat hearts were dissected out, and TG2 expression, activity, and S-nitrosation were determined. Young (6-month-old) males were used as controls. TG2 activity significantly increased in the saline-treated but not in the cystamine-treated aging rat hearts. TG2 expression also increased with age and was unaltered by cystamine treatment. Aged rats showed increased left ventricular (LV) end-systolic dimension and a decrease in fractional shortening compared with young, which was not affected by cystamine. However, cystamine treatment preserved the preload-independent index of LV filling pressure and restored end-diastolic pressure, end-diastolic pressure-volume relationships, and arterial elastance toward young. An increase in TG2 activity contributes to age-associated increase in diastolic stiffness, thereby contributing to age-associated diastolic dysfunction. TG2 may thus represent a novel target for age-associated diastolic heart failure.

show abstract