Role of calcium in pathogenesis of acute renal failure
H. D. Humes The potential for calcium to play a key role in cell injury has been long suspected. Major sites of calcium action to promote cell injury include the plasma membrane, mitochondria, endoplasmic reticulum, and the cytoskeleton. Major mechanisms of calcium action to promote cell injury incl...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 1986-04, Vol.250 (4), p.579-F589 |
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| container_issue | 4 |
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| container_title | American journal of physiology. Renal physiology |
| container_volume | 250 |
| creator | Humes, H. D |
| description | H. D. Humes
The potential for calcium to play a key role in cell injury has been long
suspected. Major sites of calcium action to promote cell injury include the
plasma membrane, mitochondria, endoplasmic reticulum, and the cytoskeleton.
Major mechanisms of calcium action to promote cell injury include
activation of phospholipases, direct and indirect effects on permeability
pathways, and effects on contractile and cytoskeletal structure and
function. The activation of phospholipases and deterioration of
mitochondrial structure and function by calcium appear to be most important
in the evolution of cell injury. Tissue calcium levels invariably increase
when lethal cell injury develops in a tissue and is due predominantly to
mitochondrial accumulation and sequestration. The simultaneous occurrence
of cell calcium overload and lethal cell injury, however, only establishes
an association between these two events but does not prove causality. Over
the past several years, a large amount of data has established that calcium
plays a critical modifying role in the pathogenesis of both ischemic and
toxic cell injury, but evidence for the thesis that calcium is the "final
common pathway" for lethal cell injury is not conclusive. Many studies have
emphasized the role of calcium influx from extracellular to intracellular
spaces with resulting cellular calcium overload in cell injury. A critical
role for intracellular redistribution of calcium pools rather than cellular
calcium influx during the important early stages of cell injury may be more
important. Modifying alterations in cell calcium redistribution or cellular
calcium influx with a variety of agents has been beneficial in ameliorating
the degree of cell injury in a number of experimental settings. It is still
unclear whether these beneficial effects are due mainly to alterations of
calcium-mediated processes that determine the reversibility of injury or
are due to alterations in other critical metabolic processes not
importantly influenced by calcium. |
| doi_str_mv | 10.1152/ajprenal.1986.250.4.f579 |
| format | Article |
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The potential for calcium to play a key role in cell injury has been long
suspected. Major sites of calcium action to promote cell injury include the
plasma membrane, mitochondria, endoplasmic reticulum, and the cytoskeleton.
Major mechanisms of calcium action to promote cell injury include
activation of phospholipases, direct and indirect effects on permeability
pathways, and effects on contractile and cytoskeletal structure and
function. The activation of phospholipases and deterioration of
mitochondrial structure and function by calcium appear to be most important
in the evolution of cell injury. Tissue calcium levels invariably increase
when lethal cell injury develops in a tissue and is due predominantly to
mitochondrial accumulation and sequestration. The simultaneous occurrence
of cell calcium overload and lethal cell injury, however, only establishes
an association between these two events but does not prove causality. Over
the past several years, a large amount of data has established that calcium
plays a critical modifying role in the pathogenesis of both ischemic and
toxic cell injury, but evidence for the thesis that calcium is the "final
common pathway" for lethal cell injury is not conclusive. Many studies have
emphasized the role of calcium influx from extracellular to intracellular
spaces with resulting cellular calcium overload in cell injury. A critical
role for intracellular redistribution of calcium pools rather than cellular
calcium influx during the important early stages of cell injury may be more
important. Modifying alterations in cell calcium redistribution or cellular
calcium influx with a variety of agents has been beneficial in ameliorating
the degree of cell injury in a number of experimental settings. It is still
unclear whether these beneficial effects are due mainly to alterations of
calcium-mediated processes that determine the reversibility of injury or
are due to alterations in other critical metabolic processes not
importantly influenced by calcium.</description><identifier>ISSN: 0363-6127</identifier><identifier>ISSN: 0002-9513</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 2161-1157</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.1986.250.4.f579</identifier><identifier>PMID: 3515968</identifier><language>eng</language><publisher>United States</publisher><subject>Acute Kidney Injury - physiopathology ; Aminoglycosides - toxicity ; Animals ; Calcium - physiology ; Cell Compartmentation ; Cell Membrane - physiology ; Cell Membrane Permeability ; Intracellular Membranes - physiology ; Ischemia - physiopathology ; Kidney - blood supply ; Kidney - drug effects ; Kidney - metabolism ; Mitochondria - physiology</subject><ispartof>American journal of physiology. Renal physiology, 1986-04, Vol.250 (4), p.579-F589</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-64457c5db69d31f30d7b68c646a2e4d85161e9a789141e2b69bb6bfe2487b0333</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3515968$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Humes, H. D</creatorcontrib><title>Role of calcium in pathogenesis of acute renal failure</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol</addtitle><description>H. D. Humes
The potential for calcium to play a key role in cell injury has been long
suspected. Major sites of calcium action to promote cell injury include the
plasma membrane, mitochondria, endoplasmic reticulum, and the cytoskeleton.
Major mechanisms of calcium action to promote cell injury include
activation of phospholipases, direct and indirect effects on permeability
pathways, and effects on contractile and cytoskeletal structure and
function. The activation of phospholipases and deterioration of
mitochondrial structure and function by calcium appear to be most important
in the evolution of cell injury. Tissue calcium levels invariably increase
when lethal cell injury develops in a tissue and is due predominantly to
mitochondrial accumulation and sequestration. The simultaneous occurrence
of cell calcium overload and lethal cell injury, however, only establishes
an association between these two events but does not prove causality. Over
the past several years, a large amount of data has established that calcium
plays a critical modifying role in the pathogenesis of both ischemic and
toxic cell injury, but evidence for the thesis that calcium is the "final
common pathway" for lethal cell injury is not conclusive. Many studies have
emphasized the role of calcium influx from extracellular to intracellular
spaces with resulting cellular calcium overload in cell injury. A critical
role for intracellular redistribution of calcium pools rather than cellular
calcium influx during the important early stages of cell injury may be more
important. Modifying alterations in cell calcium redistribution or cellular
calcium influx with a variety of agents has been beneficial in ameliorating
the degree of cell injury in a number of experimental settings. It is still
unclear whether these beneficial effects are due mainly to alterations of
calcium-mediated processes that determine the reversibility of injury or
are due to alterations in other critical metabolic processes not
importantly influenced by calcium.</description><subject>Acute Kidney Injury - physiopathology</subject><subject>Aminoglycosides - toxicity</subject><subject>Animals</subject><subject>Calcium - physiology</subject><subject>Cell Compartmentation</subject><subject>Cell Membrane - physiology</subject><subject>Cell Membrane Permeability</subject><subject>Intracellular Membranes - physiology</subject><subject>Ischemia - physiopathology</subject><subject>Kidney - blood supply</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Mitochondria - physiology</subject><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><issn>2161-1157</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkFtLwzAUx4Moc04_gpAv0Jp700cZzgkDQfQ5JGmyZnRrSVZk397MzcvTefhfzjk_ACBGJcacPOjNEN1OdyWupSgJRyUrPa_qCzAlWOAim6pLMEVU0EJgUl2Dm5Q2CBEipJiACeWY10JOgXjrOwd7D63ubBi3MOzgoPdtv3Y7l0I6StqOewe_90GvQzdGdwuuvO6SuzvPGfhYPL3Pl8Xq9fll_rgqLMN8XwjGeGV5Y0TdUOwpaiojpBVMaOJYI3m-1dW6kjVm2JFsM0YY7wiTlUGU0hmQp14b-5Si82qIYavjQWGkjiTUDwl1JKEyCcXUIpPI0ftTdBjN1jW_wfPrWS9PehvW7WeITg3tIYW-69eHv9Z_hV_w2Wxr</recordid><startdate>19860401</startdate><enddate>19860401</enddate><creator>Humes, H. D</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19860401</creationdate><title>Role of calcium in pathogenesis of acute renal failure</title><author>Humes, H. D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-64457c5db69d31f30d7b68c646a2e4d85161e9a789141e2b69bb6bfe2487b0333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Acute Kidney Injury - physiopathology</topic><topic>Aminoglycosides - toxicity</topic><topic>Animals</topic><topic>Calcium - physiology</topic><topic>Cell Compartmentation</topic><topic>Cell Membrane - physiology</topic><topic>Cell Membrane Permeability</topic><topic>Intracellular Membranes - physiology</topic><topic>Ischemia - physiopathology</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Mitochondria - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Humes, H. D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Humes, H. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of calcium in pathogenesis of acute renal failure</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1986-04-01</date><risdate>1986</risdate><volume>250</volume><issue>4</issue><spage>579</spage><epage>F589</epage><pages>579-F589</pages><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><eissn>2161-1157</eissn><eissn>1522-1466</eissn><abstract>H. D. Humes
The potential for calcium to play a key role in cell injury has been long
suspected. Major sites of calcium action to promote cell injury include the
plasma membrane, mitochondria, endoplasmic reticulum, and the cytoskeleton.
Major mechanisms of calcium action to promote cell injury include
activation of phospholipases, direct and indirect effects on permeability
pathways, and effects on contractile and cytoskeletal structure and
function. The activation of phospholipases and deterioration of
mitochondrial structure and function by calcium appear to be most important
in the evolution of cell injury. Tissue calcium levels invariably increase
when lethal cell injury develops in a tissue and is due predominantly to
mitochondrial accumulation and sequestration. The simultaneous occurrence
of cell calcium overload and lethal cell injury, however, only establishes
an association between these two events but does not prove causality. Over
the past several years, a large amount of data has established that calcium
plays a critical modifying role in the pathogenesis of both ischemic and
toxic cell injury, but evidence for the thesis that calcium is the "final
common pathway" for lethal cell injury is not conclusive. Many studies have
emphasized the role of calcium influx from extracellular to intracellular
spaces with resulting cellular calcium overload in cell injury. A critical
role for intracellular redistribution of calcium pools rather than cellular
calcium influx during the important early stages of cell injury may be more
important. Modifying alterations in cell calcium redistribution or cellular
calcium influx with a variety of agents has been beneficial in ameliorating
the degree of cell injury in a number of experimental settings. It is still
unclear whether these beneficial effects are due mainly to alterations of
calcium-mediated processes that determine the reversibility of injury or
are due to alterations in other critical metabolic processes not
importantly influenced by calcium.</abstract><cop>United States</cop><pmid>3515968</pmid><doi>10.1152/ajprenal.1986.250.4.f579</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6127 |
| ispartof | American journal of physiology. Renal physiology, 1986-04, Vol.250 (4), p.579-F589 |
| issn | 0363-6127 0002-9513 1931-857X 2161-1157 1522-1466 |
| language | eng |
| recordid | cdi_highwire_physiology_ajprenal_250_4_F579 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Acute Kidney Injury - physiopathology Aminoglycosides - toxicity Animals Calcium - physiology Cell Compartmentation Cell Membrane - physiology Cell Membrane Permeability Intracellular Membranes - physiology Ischemia - physiopathology Kidney - blood supply Kidney - drug effects Kidney - metabolism Mitochondria - physiology |
| title | Role of calcium in pathogenesis of acute renal failure |
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