International Review of Cell and Molecular Biology 

About: International Review of Cell and Molecular Biology is an academic journal published by Elsevier BV. The journal publishes majorly in the area(s): Biology & Medicine. It has an ISSN identifier of 1937-6448. Over the lifetime, 756 publications have been published receiving 31154 citations. The journal is also known as: Int Rev Cell Mol Biol.

Cell Biology of Ischemia/Reperfusion Injury

Abstract: Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues.

Endoplasmic reticulum and the unfolded protein response: dynamics and metabolic integration.

Abstract: The endoplasmic reticulum (ER) is a dynamic intracellular organelle with multiple functions essential for cellular homeostasis, development, and stress responsiveness. In response to cellular stress, a well-established signaling cascade, the unfolded protein response (UPR), is activated. This intricate mechanism is an important means of re-establishing cellular homeostasis and alleviating the inciting stress. Now, emerging evidence has demonstrated that the UPR influences cellular metabolism through diverse mechanisms, including calcium and lipid transfer, raising the prospect of involvement of these processes in the pathogenesis of disease, including neurodegeneration, cancer, diabetes mellitus and cardiovascular disease. Here, we review the distinct functions of the ER and UPR from a metabolic point of view, highlighting their association with prevalent pathologies.

Photoinhibition of Photosystem II

Abstract: Photoinhibition of Photosystem II (PSII) is the light-induced loss of PSII electron-transfer activity. Although photoinhibition has been studied for a long time, there is no consensus about its mechanism. On one hand, production of singlet oxygen ((1)O(2)) by PSII has promoted models in which this reactive oxygen species (ROS) is considered to act as the agent of photoinhibitory damage. These chemistry-based models have often not taken into account the photophysical features of photoinhibition-like light response and action spectrum. On the other hand, models that reproduce these basic photophysical features of the reaction have not considered the importance of data about ROS. In this chapter, it is shown that the evidence behind the chemistry-based models and the photophysically oriented models can be brought together to build a mechanism that confirms with all types of experimental data. A working hypothesis is proposed, starting with inhibition of the manganese complex by light. Inability of the manganese complex to reduce the primary donor promotes recombination between the oxidized primary donor and Q(A), the first stable quinone acceptor of PSII. (1)O(2) production due to this recombination may inhibit protein synthesis or spread the photoinhibitory damage to another PSII center. The production of (1)O(2) is transient because loss of activity of the oxygen-evolving complex induces an increase in the redox potential of Q(A), which lowers (1)O(2) production.

Lipid rafts, caveolae, and their endocytosis.

Abstract: Lipid rafts are plasma membrane microdomains enriched in cholesterol and sphingolipids that are involved in the lateral compartmentalization of molecules at the cell surface. Internalization of ligands and receptors by these domains occurs via a process defined as raft-dependent endocytosis. Caveolae are caveolin-1-enriched smooth invaginations of the plasma membrane that form a subdomain of lipid rafts. Endocytosis of rafts, including caveolar but also noncaveolar dynamin-dependent and dynamin-independent pathways, is characterized by its cholesterol sensitivity and clathrin-independence. In this review we will characterize lipid rafts and caveolae, their endocytosis and its regulation by the actin cytoskeleton, caveolin-1, dynamin, and cholesterol.

NF-κB and the Transcriptional Control of Inflammation.

Abstract: The NF-κB transcription factor was discovered 30 years ago and has since emerged as the master regulator of inflammation and immune homeostasis. It achieves this status by means of the large number of important pro- and antiinflammatory factors under its transcriptional control. NF-κB has a central role in inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and autoimmunity, as well as diseases comprising a significant inflammatory component such as cancer and atherosclerosis. Here, we provide an overview of the studies that form the basis of our understanding of the role of NF-κB subunits and their regulators in controlling inflammation. We also describe the emerging importance of posttranslational modifications of NF-κB in the regulation of inflammation, and highlight the future challenges faced by researchers who aim to target NF-κB transcriptional activity for therapeutic benefit in treating chronic inflammatory diseases.