Age-related changes of myocardial ATP supply and demand mechanisms

Yaniv, Yael; Juhaszova, Magdalena; Sollott, Steven J.

doi:10.1016/j.tem.2013.06.001

Cited by 48 publications

(32 citation statements)

References 89 publications

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“…Compared with young cells, aging mitochondria generate more ROS, and furthermore, aging cells are progressively susceptible to mitochondria derived ROS. While it has been known since the 1960s that mitochondria produce ROS (Jensen, 1966), the production of ROS by mitochondrial ETC complexes had not been fully elucidated until relatively recently (Yaniv et al, 2013; Zorov et al, 2005). Under physiological conditions during ATP synthesis, the ETC complexes generate ROS that leak out of the mitochondrial membrane (Chen et al, 2012; Liu et al, 2002; Murphy, 2009).…”

Section: Oxidative Stress: When Does a Friend Become A Foe?mentioning

confidence: 99%

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Datta

Cano

Ebrahimi

et al. 2017

Progress in Retinal and Eye Research

593

487

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The retinal pigment epithelium (RPE) is a highly specialized, unique epithelial cell that interacts with photoreceptors on its apical side and with Bruch’s membrane and the choriocapillaris on its basal side. Due to vital functions that keep photoreceptors healthy, the RPE is essential for maintaining vision. With aging and the accumulated effects of environmental stresses, the RPE can become dysfunctional and die. This degeneration plays a central role in age-related macular degeneration (AMD) pathobiology, the leading cause of blindness among the elderly in western societies. Oxidative stress and inflammation have both physiological and potentially pathological roles in RPE degeneration. Given the central role of the RPE, this review will focus on the impact of oxidative stress and inflammation on the RPE with AMD pathobiology. Physiological sources of oxidative stress as well as unique sources from photo-oxidative stress, the phagocytosis of photoreceptor outer segments, and modifiable factors such as cigarette smoking and high fat diet ingestion that can convert oxidative stress into a pathological role, and the negative impact of impairing the cytoprotective roles of mitochondrial dynamics and the Nrf2 signaling system on RPE health in AMD will be discussed. Likewise, the response by the innate immune system to an inciting trigger, and the potential role of local RPE production of inflammation, as well as a potential role for damage by inflammation with chronicity if the inciting trigger is not neutralized, will be debated.

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Section: Oxidative Stress: When Does a Friend Become A Foe?mentioning

confidence: 99%

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Datta

Cano

Ebrahimi

et al. 2017

Progress in Retinal and Eye Research

593

487

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“…They have also often only been studied in adult and not aged tissues. This could account for discrepancies in the literature regarding age-related changes in cardiac Ca 2ϩ cycling proteins (23,58). The present study analyzed protein expression in the different dissected mouse heart tissues, thereby allowing identification of important regional differences.…”

Section: Reduced Response Of the Aged San To Neurotransmittersmentioning

confidence: 99%

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

Liu

Sirenko

Juhaszova

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Lakatta EG. Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca 2ϩ signaling. Am J Physiol Heart Circ Physiol 306: H1385-H1397, 2014. First published March 14, 2014 doi:10.1152/ajpheart.00088.2014.-A reduced sinoatrial node (SAN) functional reserve underlies the age-associated decline in heart rate acceleration in response to stress. SAN cell function involves an oscillatory coupled-clock system: the sarcoplasmic reticulum (SR), a Ca 2ϩ clock, and the electrogenic-sarcolemmal membrane clock. Ca 2ϩ -activated-calmodulin-adenylyl cyclase/CaMKII-cAMP/PKA-Ca 2ϩ signaling regulated by phosphodiesterase activity drives SAN cells automaticity. SR-generated local calcium releases (LCRs) activate Na ϩ /Ca 2ϩ exchanger in the membrane clock, which initiates the action potential (AP). We hypothesize that SAN cell dysfunctions accumulate with age. We found a reduction in single SAN cell AP firing in aged (20 -24 mo) vs. adult (3-4 mo) mice. The sensitivity of the SAN beating rate responses to both muscarinic and adrenergic receptor activation becomes decreased in advanced age. Additionally, age-associated coincident dysfunctions occur stemming from compromised clock functions, including a reduced SR Ca 2ϩ load and a reduced size, number, and duration of spontaneous LCRs. Moreover, the sensitivity of SAN beating rate to a cAMP stress induced by phosphodiesterase inhibitor is reduced, as are the LCR size, amplitude, and number in SAN cells from aged vs. adult mice. These functional changes coincide with decreased expression of crucial SR Ca 2ϩ -cycling proteins, including SR Ca 2ϩ -ATPase pump, ryanodine receptors, and Na ϩ /Ca 2ϩ exchanger. Thus a deterioration in intrinsic Ca 2ϩ clock kinetics in aged SAN cells, due to deficits in intrinsic SR Ca 2ϩ cycling and its response to a cAMP-dependent pathway activation, is involved in the age-associated reduction in intrinsic resting AP firing rate, and in the reduction in the acceleration of heart rate during exercise.aging; Ca 2ϩ transient; intrinsic heart rate; pacemaker function; PKA signaling AN AGE-ASSOCIATED REDUCTION in heart rate acceleration in response to stress is a major factor underlying the age-associated decline in cardiovascular reserve (29). Specifically, the heart rate increase in response to perturbations from the supine basal state, e.g., on assuming an upright posture or during exercise, is reduced in older vs. younger persons (43). That an exaggerated increase in plasma catecholamines accompanies the reduction in heart rate reserve in older persons suggests that the age-associated reduction in heart rate reserve, in part at least, is attributable to postsynaptic mechanisms that reside within the sinoatrial node (SAN) (14). Broadly, these postsynaptic mechanisms include intrinsic mechanisms that control the rate and rhythm of spontaneous action potential (AP) firing of SAN pacemaker cells, and autonomic receptor signaling that modulates these intrinsic pacemaker cell mechanisms (3, 22, 37). The...

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“…The muscle work efficiency may vary with time even in the same muscle: Barclay and Weber (2004) after determining the work output and heat production in in vitro experiments with the slowtwitch soleus and fast-twitch extensor digitorum longus muscle fibers from mouse reported that during the first second of the experiments the efficiency was greater in the slow-twitch soleus muscle, than it was in the fast-twitch extensor digitorum longus muscle, but there was no difference in the net efficiency of the muscles in the longer time span. Yaniv et al (2013) argue that the myocardial ATP supply and demand mechanisms are age dependent.…”

Section: Comparison Of the Theoretical Limits With The Calculations Bmentioning

confidence: 99%

First and second law work production efficiency of a muscle cell

Sorgüven

Özilgen

2015

IJEX

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The absolute value of the muscle efficiency and its decrease over time has vital consequences. Among other diseases heart failure, which is the leading cause of death in developed countries is dramatically affected by muscle weakness. This paper provides an analogy between the Carnot engine and muscle to gain insight on the muscle work production process and estimate the maximum muscle efficiency under physiological conditions. An "ideal muscle" model, which operates steadily and reversibly, is defined and for this model energy and exergy analyses are performed. Theoretical results are compared with the experimental measurements.

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Age-related changes of myocardial ATP supply and demand mechanisms

Cited by 48 publications

References 89 publications

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling

First and second law work production efficiency of a muscle cell

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Age-related changes of myocardial ATP supply and demand mechanisms

Cited by 48 publications

References 89 publications

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca2+signaling

First and second law work production efficiency of a muscle cell

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Age-associated abnormalities of intrinsic automaticity of sinoatrial nodal cells are linked to deficient cAMP-PKA-Ca²⁺signaling