Targeting autophagy in cardiac ischemia/reperfusion injury: A novel therapeutic strategy
Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumu...
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| Veröffentlicht in: | Journal of cellular physiology 2019-10, Vol.234 (10), p.16768-16778 |
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| creator | Aghaei, Mehrdad Motallebnezhad, Morteza Ghorghanlu, Sajjad Jabbari, Ali Enayati, Ayesheh Rajaei, Maryam Pourabouk, Mona Moradi, Alireza Alizadeh, Ali Mohammad Khori, Vahid |
| description | Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumulation, disruption of mitochondrial membrane potential, the formation of reactive oxygen species, and so forth. One of the processes that gets activated in response to I/R injury is autophagy. Indeed, autophagy acts as a “double‐edged sword” in the pathology of myocardial I/R injury and there is a controversy about autophagy being beneficial or detrimental. On the basis of the autophagy effect and regulation on myocardial I/R injury, many studies targeted it as a therapeutic strategy. In this review, we discuss the role of autophagy in I/R injury and its targeting as a therapeutic strategy.
In this review, we discuss the role of autophagy in ischemia/reperfusion injury and its targeting as a therapeutic strategy. |
| doi_str_mv | 10.1002/jcp.28345 |
| format | Article |
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In this review, we discuss the role of autophagy in ischemia/reperfusion injury and its targeting as a therapeutic strategy.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.28345</identifier><identifier>PMID: 30807647</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>acute myocardial infarction ; Animals ; Autophagy ; Blood flow ; Cardiovascular Agents - therapeutic use ; Disruption ; Humans ; Injuries ; Ion accumulation ; Ischemia ; ischemia/reperfusion injury ; Membrane potential ; Mitochondria ; Morbidity ; Myocardial infarction ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Phagocytosis ; Reactive oxygen species ; Reperfusion ; Strategy ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>Journal of cellular physiology, 2019-10, Vol.234 (10), p.16768-16778</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4195-18493793ecef670164954a72e84c9322b8620531e55c792359755afa3563d4a03</citedby><cites>FETCH-LOGICAL-c4195-18493793ecef670164954a72e84c9322b8620531e55c792359755afa3563d4a03</cites><orcidid>0000-0001-9323-9325</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.28345$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.28345$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30807647$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aghaei, Mehrdad</creatorcontrib><creatorcontrib>Motallebnezhad, Morteza</creatorcontrib><creatorcontrib>Ghorghanlu, Sajjad</creatorcontrib><creatorcontrib>Jabbari, Ali</creatorcontrib><creatorcontrib>Enayati, Ayesheh</creatorcontrib><creatorcontrib>Rajaei, Maryam</creatorcontrib><creatorcontrib>Pourabouk, Mona</creatorcontrib><creatorcontrib>Moradi, Alireza</creatorcontrib><creatorcontrib>Alizadeh, Ali Mohammad</creatorcontrib><creatorcontrib>Khori, Vahid</creatorcontrib><title>Targeting autophagy in cardiac ischemia/reperfusion injury: A novel therapeutic strategy</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumulation, disruption of mitochondrial membrane potential, the formation of reactive oxygen species, and so forth. One of the processes that gets activated in response to I/R injury is autophagy. Indeed, autophagy acts as a “double‐edged sword” in the pathology of myocardial I/R injury and there is a controversy about autophagy being beneficial or detrimental. On the basis of the autophagy effect and regulation on myocardial I/R injury, many studies targeted it as a therapeutic strategy. In this review, we discuss the role of autophagy in I/R injury and its targeting as a therapeutic strategy.
In this review, we discuss the role of autophagy in ischemia/reperfusion injury and its targeting as a therapeutic strategy.</description><subject>acute myocardial infarction</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Blood flow</subject><subject>Cardiovascular Agents - therapeutic use</subject><subject>Disruption</subject><subject>Humans</subject><subject>Injuries</subject><subject>Ion accumulation</subject><subject>Ischemia</subject><subject>ischemia/reperfusion injury</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Morbidity</subject><subject>Myocardial infarction</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Phagocytosis</subject><subject>Reactive oxygen species</subject><subject>Reperfusion</subject><subject>Strategy</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAQhi0EoqUw8AdQJBYY0vozidmqik9VgqFIbJbrXlpXaRLsBJR_j0sLAxLTDffcc69ehM4JHhKM6Wht6iHNGBcHqE-wTGOeCHqI-mFHYik46aET79cYYykZO0Y9hjOcJjzto7eZdktobLmMdNtU9Uovu8iWkdFuYbWJrDcr2Fg9clCDy1tvqzLs163rbqJxVFYfUETNCpyuoW2siXzjdAPL7hQd5brwcLafA_R6dzubPMTT5_vHyXgaG06kiEnGJUslAwN5kmKS8JBXpxQybiSjdJ4lFAtGQAiTSsqETIXQuWYiYQuuMRugq523dtV7C75Rm5AZikKXULVeUZIlCRHhNKCXf9B11boypFOUcsnDd7wVXu8o4yrvHeSqdnajXacIVtu6Vahbfdcd2Iu9sZ1vYPFL_vQbgNEO-LQFdP-b1NPkZaf8AvNkh6M</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Aghaei, Mehrdad</creator><creator>Motallebnezhad, Morteza</creator><creator>Ghorghanlu, Sajjad</creator><creator>Jabbari, Ali</creator><creator>Enayati, Ayesheh</creator><creator>Rajaei, Maryam</creator><creator>Pourabouk, Mona</creator><creator>Moradi, Alireza</creator><creator>Alizadeh, Ali Mohammad</creator><creator>Khori, Vahid</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9323-9325</orcidid></search><sort><creationdate>201910</creationdate><title>Targeting autophagy in cardiac ischemia/reperfusion injury: A novel therapeutic strategy</title><author>Aghaei, Mehrdad ; Motallebnezhad, Morteza ; Ghorghanlu, Sajjad ; Jabbari, Ali ; Enayati, Ayesheh ; Rajaei, Maryam ; Pourabouk, Mona ; Moradi, Alireza ; Alizadeh, Ali Mohammad ; Khori, Vahid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4195-18493793ecef670164954a72e84c9322b8620531e55c792359755afa3563d4a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>acute myocardial infarction</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Blood flow</topic><topic>Cardiovascular Agents - therapeutic use</topic><topic>Disruption</topic><topic>Humans</topic><topic>Injuries</topic><topic>Ion accumulation</topic><topic>Ischemia</topic><topic>ischemia/reperfusion injury</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Morbidity</topic><topic>Myocardial infarction</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Phagocytosis</topic><topic>Reactive oxygen species</topic><topic>Reperfusion</topic><topic>Strategy</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aghaei, Mehrdad</creatorcontrib><creatorcontrib>Motallebnezhad, Morteza</creatorcontrib><creatorcontrib>Ghorghanlu, Sajjad</creatorcontrib><creatorcontrib>Jabbari, Ali</creatorcontrib><creatorcontrib>Enayati, Ayesheh</creatorcontrib><creatorcontrib>Rajaei, Maryam</creatorcontrib><creatorcontrib>Pourabouk, Mona</creatorcontrib><creatorcontrib>Moradi, Alireza</creatorcontrib><creatorcontrib>Alizadeh, Ali Mohammad</creatorcontrib><creatorcontrib>Khori, Vahid</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aghaei, Mehrdad</au><au>Motallebnezhad, Morteza</au><au>Ghorghanlu, Sajjad</au><au>Jabbari, Ali</au><au>Enayati, Ayesheh</au><au>Rajaei, Maryam</au><au>Pourabouk, Mona</au><au>Moradi, Alireza</au><au>Alizadeh, Ali Mohammad</au><au>Khori, Vahid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting autophagy in cardiac ischemia/reperfusion injury: A novel therapeutic strategy</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-10</date><risdate>2019</risdate><volume>234</volume><issue>10</issue><spage>16768</spage><epage>16778</epage><pages>16768-16778</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumulation, disruption of mitochondrial membrane potential, the formation of reactive oxygen species, and so forth. One of the processes that gets activated in response to I/R injury is autophagy. Indeed, autophagy acts as a “double‐edged sword” in the pathology of myocardial I/R injury and there is a controversy about autophagy being beneficial or detrimental. On the basis of the autophagy effect and regulation on myocardial I/R injury, many studies targeted it as a therapeutic strategy. In this review, we discuss the role of autophagy in I/R injury and its targeting as a therapeutic strategy.
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| subjects | acute myocardial infarction Animals Autophagy Blood flow Cardiovascular Agents - therapeutic use Disruption Humans Injuries Ion accumulation Ischemia ischemia/reperfusion injury Membrane potential Mitochondria Morbidity Myocardial infarction Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Phagocytosis Reactive oxygen species Reperfusion Strategy TOR Serine-Threonine Kinases - metabolism |
| title | Targeting autophagy in cardiac ischemia/reperfusion injury: A novel therapeutic strategy |
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