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Reverse electron flow (also known as reverse electron transport) is a mechanism in microbial metabolism. Chemolithotrophs using an electron donor with a higher redox potential than NAD(P)+/NAD(P)H,such as nitrite or sulfur compounds,must use energy to reduce NAD(P)+. This energy is supplied by consuming proton motive force to drive electrons in a reverse direction through an electron transport chain and is thus the reverse process as forward electron transport. In some cases,the energy consumed in reverse electron transport is five times greater than energy gained from the forward process. Autotrophs can use this process to supply reducing power for inorganic carbon fixation.
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Nix is a pro-apoptotic gene that is regulated by Histotoxic hypoxia. It expresses a signaling protein related to the BH3-only family. This protein induces autophagy,an intracellular function by which cytoplasmic components are delivered to the lysosome to be broken down and used elsewhere or excreted from the cell. This protein is important in development because it allows cells to have a consistent store of cellular components. It also holds an important role in the differentiation and maturation of erythrocytes and lymphocytes by the process of mitophagy with the help of its regulator BNIP3. Using a gene knockout technique in mice,scientists have been able to attribute this pruning of mitochondria and induction of cellular necrosis to the expression of the Nix gene. The Nix protein may be associated with certain kinds of cancer formation. In mouse models,loss of Nix resulted in a delayed onset of tumors for pancreatic cancer,and was additionally associated with reduced mitophagy and increased oxidative metabolism. Nix therefore may be a tumor promoter for pancreatic cancer.
Cardioprotection includes all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage. Cardioprotection encompasses several regimens that have shown to preserve function and viability of cardiac muscle cell tissue subjected to ischemic insult or reoxygenation. Cardioprotection includes strategies that are implemented before an ischemic event,during an ischemic event and after the event and during reperfusion. These strategies can be further stratified by performing the intervention locally or remotely,creating classes of conditioning known as remote ischemic PC (RIPC),remote ischemic PostC and remost ischemic PerC. Classical (local) preconditioning has an early phase with an immediate onset lasting 2–3 hours that protects against myocardial infarction. The early phase involves post-translational modification of preexisting proteins,brought about by the activation of G protein-coupled receptors as well as downstream MAPK's and PI3/Akt. These signaling events act on the ROS-generating mitochondria,activate PKCεand the Reperfusion Injury Salvage Kinase (RISK) pathway,preventing mitochondrial permeability transition pore (MTP) opening. The late phase with an onset of 12–24 hours that lasts 3–4 days and protects against both infarction and reversible postischemic contractile dysfunction,termed myocardial stunning. This phase involves the synthesis of new cardioprotective proteins stimulated by nitric oxide (NO),ROS and adenosine acting on kinases such as PKCεand Src,which in turn activate gene transcription and upregulation of late PC molecular players.
Perilipin 5,also known as Oxpatperilipin 5 or PLIN5,is a protein that belongs to perilipin family. This protein group has been shown to be responsible for lipid droplet's biogenesis,structure and degradation. In particular,Perilipin 5 is a lipid droplet-associated protein whose function is to keep the balance between lipolysis and lipogenesis,as well as maintaining lipid droplet homeostasis. For example,in oxidative tissues,muscular tissues and cardiac tissues,PLIN5 promotes association between lipid droplets and mitochondria.
Kidney ischemia is a disease with a high morbidity and mortality rate. Blood vessels shrink and undergo apoptosis which results in poor blood flow in the kidneys. More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock,hypovolemia,and a need for surgery. What causes kidney ischemia is not entirely known,but several pathophysiology relating to this disease have been elucidated. Possible causes of kidney ischemia include the activation of IL-17C and hypoxia due to surgery or transplant. Several signs and symptoms include injury to the microvascular endothelium,apoptosis of kidney cells due to overstress in the endoplasmic reticulum,dysfunctions of the mitochondria,autophagy,inflammation of the kidneys,and maladaptive repair.
References
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