Apoptosis as a potential mechanism of muscle cachexia in chronic obstructive pulmonary disease
Humans; Biopsy; Morbidity; Pulmonary Disease; Apoptosis; Cachexia/etiology/pathology/physiopathology; Cell Nucleus/pathology; Chronic Obstructive/complications; Exercise Tolerance; Inflammation; Mitochondria; Muscle Fibers/pathology; Muscle/pathology; Muscular Atrophy/etiology/pathology/physiopathology; Sarcomeres/pathology
2002
Lewis MI
American Journal Of Respiratory And Critical Care Medicine : An Official Journal Of The American Thoracic Society, Medical Section Of The American Lung Association
2002
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1164/rccm.2205023" target="_blank" rel="noreferrer">10.1164/rccm.2205023</a>
The final step in programmed cell death: phagocytes carry apoptotic cells to the grave.
Animals; Models; Receptors; Signal Transduction; Molecular; Inflammation/metabolism; Apoptosis; Phagocytosis; Biological; Caenorhabditis elegans/genetics; Cell Surface/me [Metabolism]; Drosophila melanogaster/genetics; Evolution; Mice/genetics; Phagocytes/physiology
As cells undergo apoptosis, they are recognized and removed from the body by phagocytes. This oft-overlooked yet critical final step in the cell-death programme protects tissues from exposure to the toxic contents of dying cells and also serves to prevent further tissue damage by stimulating production of anti-inflammatory cytokines and chemokines. The clearance of apoptotic-cell corpses occurs throughout the lifespan of multicellular organisms and is important for normal development during embryogenesis, the maintenance of normal tissue integrity and function, and the resolution of inflammation. Many of the signal-transduction molecules implicated in the phagocytosis of apoptotic cells appear to have a high degree of evolutionary conservation, and therefore the engulfment of apoptotic cells is likely to represent one of the most primitive forms of phagocytosis. With the realization that the signals that govern apoptotic-cell removal also serve to attenuate inflammation and the immune response, as well as initiate signals for tissue repair and remodelling in response to cell death, the study of apoptotic cell clearance is a field experiencing a dynamic increase in interest and momentum.
2003
deCathelineau AM; Henson PM
Essays In Biochemistry
2003
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1042/bse0390105" target="_blank" rel="noreferrer">10.1042/bse0390105</a>
Bisphosphonate mechanism of action
Humans; Clodronate; Apoptosis; Bone Resorption/metabolism; Diphosphonates/chemistry/metabolism/pharmacology; Mevalonic Acid/antagonists & inhibitors; Osteoclasts/drug effects/metabolism/physiology; Osteoporosis/metabolism
The nitrogen-containing bisphosphonates (N-BPs), alendronate and risedronate, are the only pharmacologic agents shown to prevent spine and nonvertebral fractures associated with postmenopausal and glucocorticoid-induced osteoporosis. At the tissue level, this is achieved through osteoclast inhibition, which leads to reduced bone turnover, increased bone mass, and improved mineralization. The molecular targets of bisphosphonates (BPs) have recently been identified. This review will discuss the mechanism of action of BPs, focusing on alendronate and risedronate, which are the two agents most widely studied. They act on the cholesterol biosynthesis pathway enzyme, farnesyl diphosphate synthase. By inhibiting this enzyme in the osteoclast, they interfere with geranylgeranylation (attachment of the lipid to regulatory proteins), which causes osteoclast inactivation. This mechanism is responsible for N-BP suppression of osteoclastic bone resorption and reduction of bone turnover, which leads to fracture prevention.
2003
Reszka AA; Rodan GA
Current Rheumatology Reports
2003
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1007/s11926-003-0085-6" target="_blank" rel="noreferrer">10.1007/s11926-003-0085-6</a>