Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized by abnormal scarring of the lung parenchyma. There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations tha...
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| Veröffentlicht in: | The Journal of clinical investigation 2017-02, Vol.127 (2), p.405-414 |
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| creator | Mora, Ana L Bueno, Marta Rojas, Mauricio |
| description | Idiopathic pulmonary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized by abnormal scarring of the lung parenchyma. There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence. These divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-related diseases such as IPF. Therapeutic approaches that target aging processes may be beneficial for halting the progression of disease and improving quality of life in IPF patients. |
| doi_str_mv | 10.1172/JCI87440 |
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There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence. These divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-related diseases such as IPF. Therapeutic approaches that target aging processes may be beneficial for halting the progression of disease and improving quality of life in IPF patients.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/JCI87440</identifier><identifier>PMID: 28145905</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Age ; Age factors in disease ; Aging ; Aging - metabolism ; Aging - pathology ; Animals ; Apoptosis ; Autophagy ; Biomedical research ; Biosynthesis ; Care and treatment ; Chronic illnesses ; Chronic obstructive pulmonary disease ; Development and progression ; Exercise ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Genetic aspects ; Health aspects ; Homeostasis ; Humans ; Idiopathic Pulmonary Fibrosis - metabolism ; Idiopathic Pulmonary Fibrosis - pathology ; Industrialized nations ; Lung - metabolism ; Lung - pathology ; Lung diseases ; Lungs ; Mitochondria ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial DNA ; Mortality ; Older people ; Population ; Pulmonary fibrosis ; Quality of life ; Repair & maintenance ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; Review ; Rodents ; Senescence ; Studies ; Text editing</subject><ispartof>The Journal of clinical investigation, 2017-02, Vol.127 (2), p.405-414</ispartof><rights>COPYRIGHT 2017 American Society for Clinical Investigation</rights><rights>Copyright American Society for Clinical Investigation Feb 2017</rights><rights>Copyright © 2017, American Society for Clinical Investigation 2017 American Society for Clinical Investigation</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c742t-3a37c8cae4b8cbdde6780017d03dc55a94696bde0b340e9b7130a47ceeec5d4a3</citedby><cites>FETCH-LOGICAL-c742t-3a37c8cae4b8cbdde6780017d03dc55a94696bde0b340e9b7130a47ceeec5d4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5272191/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5272191/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28145905$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mora, Ana L</creatorcontrib><creatorcontrib>Bueno, Marta</creatorcontrib><creatorcontrib>Rojas, Mauricio</creatorcontrib><title>Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Idiopathic pulmonary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized by abnormal scarring of the lung parenchyma. There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence. These divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-related diseases such as IPF. Therapeutic approaches that target aging processes may be beneficial for halting the progression of disease and improving quality of life in IPF patients.</description><subject>Age</subject><subject>Age factors in disease</subject><subject>Aging</subject><subject>Aging - metabolism</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biomedical research</subject><subject>Biosynthesis</subject><subject>Care and treatment</subject><subject>Chronic illnesses</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Development and progression</subject><subject>Exercise</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - pathology</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Idiopathic Pulmonary Fibrosis - metabolism</subject><subject>Idiopathic Pulmonary Fibrosis - pathology</subject><subject>Industrialized nations</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial DNA</subject><subject>Mortality</subject><subject>Older people</subject><subject>Population</subject><subject>Pulmonary fibrosis</subject><subject>Quality of life</subject><subject>Repair & maintenance</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>Review</subject><subject>Rodents</subject><subject>Senescence</subject><subject>Studies</subject><subject>Text editing</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><recordid>eNqN0l9r1TAUAPAiirtOwU8gBUHmQ2fSpE36IozLdFcmA_-9hjQ5bTPapGtS0W9vindzlfsw8hBIfjmcnHOS5CVGpxiz_N2n7Y4zStGjZIOLgmc8J_xxskEox1nFCD9Knnl_jRCmtKBPk6OcY1pUqNgkF59NcKpzVk9GpsamoYPUjy70pu1C6ppUtsa2qbQ6Ndq4UYbOqHSc-8FZOf1OG1NPzhv_PHnSyN7Di_1-nHz_cP5te5FdXn3cbc8uM8VoHjIiCVNcSaA1V7XWUDIe82IaEa2KQla0rMpaA6oJRVDVDBMkKVMAoApNJTlO3v-NO871AFqBDZPsxTiZIaYjnDRifWNNJ1r3UxQ5y3GFY4CTfYDJ3czggxiMV9D30oKbvcCcxZQ4QeQBtCQM5bxa6Ov_6LWbJxsrsShWsbzE_J9qZQ_C2MbFFNUSVJxRjghfmhJVdkC1YCH-x1loTDxe-dMDPi4Ng1EHH7xdPYgmwK_Qytl7sfv65eH26sfavrlnO5B96Lzr52Cc9Wu4L6yKs-MnaO76h5FYJlrcTnSkr-73-w7ejjD5AzeB7FQ</recordid><startdate>20170201</startdate><enddate>20170201</enddate><creator>Mora, Ana L</creator><creator>Bueno, Marta</creator><creator>Rojas, Mauricio</creator><general>American Society for Clinical Investigation</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20170201</creationdate><title>Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis</title><author>Mora, Ana L ; Bueno, Marta ; Rojas, Mauricio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c742t-3a37c8cae4b8cbdde6780017d03dc55a94696bde0b340e9b7130a47ceeec5d4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Age</topic><topic>Age factors in disease</topic><topic>Aging</topic><topic>Aging - 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There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence. These divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which potentiate maladaptation to stress and susceptibility to age-related diseases such as IPF. Therapeutic approaches that target aging processes may be beneficial for halting the progression of disease and improving quality of life in IPF patients.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>28145905</pmid><doi>10.1172/JCI87440</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Age Age factors in disease Aging Aging - metabolism Aging - pathology Animals Apoptosis Autophagy Biomedical research Biosynthesis Care and treatment Chronic illnesses Chronic obstructive pulmonary disease Development and progression Exercise Fibroblasts - metabolism Fibroblasts - pathology Genetic aspects Health aspects Homeostasis Humans Idiopathic Pulmonary Fibrosis - metabolism Idiopathic Pulmonary Fibrosis - pathology Industrialized nations Lung - metabolism Lung - pathology Lung diseases Lungs Mitochondria Mitochondria - metabolism Mitochondria - pathology Mitochondrial DNA Mortality Older people Population Pulmonary fibrosis Quality of life Repair & maintenance Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Review Rodents Senescence Studies Text editing |
| title | Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis |
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