1,721,066 research outputs found
Altered Mitochondrial Metabolism and Mechanosensation in the Failing Heart: Focus on Intracellular Calcium Signaling
No full textThe heart consists of millions of cells, namely cardiomyocytes, which are highly organized in terms of structure and function, at both macroscale and microscale levels. Such meticulous organization is imperative for assuring the physiological pump-function of the heart. One of the key players for the electrical and mechanical synchronization and contraction is the calcium ion via the well-known calcium-induced calcium release process. In cardiovascular diseases, the structural organization is lost, resulting in morphological, electrical, and metabolic remodeling owing the imbalance of the calcium handling and promoting heart failure and arrhythmias. Recently, attention has been focused on the role of mitochondria, which seem to jeopardize these events by misbalancing the calcium processes. In this review, we highlight our recent findings, especially the role of mitochondria (dys)function in failing cardiomyocytes with respect to the calcium machinery
Mitochondrial mechanosensor microdomains in cardiovascular disorders
No full textThe cardiomyocytes populating the ‘working myocardium’ are highly organized and such organization ranges from macroscale (e.g. the geometrical rod shape) to microscale (dyad/t-tubules) domains. This meticulous level of organization is imperative for assuring the normal and physiological pump-function of the heart. In the pathological cardiac tissue, the domains-related architecture is partially lost, resulting in morphological, electrical and metabolic remodeling and promoting cardiovascular diseases including heart failure and arrhythmias. Indeed, arrhythmogenesis during heart failure is a major clinical problem. Arrhythmias have been extensively studied from an electrical etiology, but only recently, physiologists and scientists have focused their attention on cellular and subcellular mechanosensors. We and others have investigated whether the nanoscale mechanosensitive properties of cardiomyocytes from failing hearts have a bearing upon the initiation of abnormal electrical activity. This chapter highlights the recent findings in the field, especially the role of mitochondria function and alignment in failing cardiomyocytes interrogated via nanomechanical stimuli
Specific nutritional problems in acute kidney injury, treated with non-dialysis and dialytic modalities
No full textPatients who develop AKI, especially in the intensive care
unit (ICU), are at risk of protein–energy malnutrition,which
is a major negative prognostic factor in this clinical condition.
Despite the lack of evidence from controlled trials
of its effect on outcome, nutritional support by the enteral
(preferentially) and/or parenteral route appears clinically indicated
in most cases of ICU-acquired AKI, independently
of the actual nutritional status of the patient, in order to prevent
deterioration in the nutritional state with all its known
complications. Extrapolating from data in other conditions,
it seems intrinsically unlikely that starvation of a catabolic
patient is more beneficial than appropriate nutritional support
by an expert team with the skills to avoid the potential
complications of the enteral and parenteral nutrition
methodologies. By the same token, it is ethically impossible
to conduct a trial in which the control group undergoes
prolonged starvation. The primary goals of nutritional support
in AKI, which represents a well-known inflammatory
and pro-oxidative condition, are the same as those for other
critically ill patients with normal renal function, i.e. to ensure
the delivery of adequate nutrition, to prevent protein–
energy wasting with its attendant metabolic complications,
to promote wound healing and tissue repair, to support immune
system function, to accelerate recovery and to reduce
mortality. Patients with AKI on RRT should receive a basic
intake of at least 1.5 g/kg/day of protein with an additional
0.2 g/kg/day to compensate for amino acid/protein
loss during RRT, especially when daily treatments and/or
high efficiecy modalities are used. Energy intake should
consist of no more than 30 kcal non-protein calories or
1.3 × BEE (Basal Energy Expenditure) calculated by the
Harris–Benedict equation, with ∼30–35% from lipid, as
lipid emulsions. For nutritional support, the enteral route
is preferred, although it often needs to be supplemented
through the parenteral route in order to meet nutritional
requirement
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