Pathophysiology of heart failure and frailty: a common inflammatory origin?
Summary Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammat...
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Veröffentlicht in: | Aging cell 2017-06, Vol.16 (3), p.444-450 |
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description | Summary
Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF. |
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Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF.</description><identifier>ISSN: 1474-9718</identifier><identifier>EISSN: 1474-9726</identifier><identifier>DOI: 10.1111/acel.12581</identifier><identifier>PMID: 28266167</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Age ; Aged ; Aging - genetics ; Aging - immunology ; Aging - pathology ; Animals ; C-Reactive Protein - genetics ; C-Reactive Protein - immunology ; Cytokines ; Cytokines - genetics ; Cytokines - immunology ; Frail Elderly ; Frailty ; Frailty - genetics ; Frailty - immunology ; Frailty - physiopathology ; Gene Expression Regulation - immunology ; Gerontology ; Heart diseases ; Heart failure ; Heart Failure - genetics ; Heart Failure - immunology ; Heart Failure - pathology ; Humans ; Immunity, Innate ; Inflammation ; pathophysiology ; Review ; Reviews ; Sarcopenia ; Sarcopenia - genetics ; Sarcopenia - immunology ; Sarcopenia - pathology ; Signal Transduction ; Toll-Like Receptors - genetics ; Toll-Like Receptors - immunology</subject><ispartof>Aging cell, 2017-06, Vol.16 (3), p.444-450</ispartof><rights>2017 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.</rights><rights>2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 The Anatomical Society and John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5811-c6fdfc05d18b2b2f4b5c114c0aa8652af9e00575df616c6bb3a62e529f6067943</citedby><cites>FETCH-LOGICAL-c5811-c6fdfc05d18b2b2f4b5c114c0aa8652af9e00575df616c6bb3a62e529f6067943</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/PMC5418206/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418206/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1416,11560,27922,27923,45572,45573,46050,46474,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28266167$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bellumkonda, Lavanya</creatorcontrib><creatorcontrib>Tyrrell, Daniel</creatorcontrib><creatorcontrib>Hummel, Scott L.</creatorcontrib><creatorcontrib>Goldstein, Daniel R.</creatorcontrib><title>Pathophysiology of heart failure and frailty: a common inflammatory origin?</title><title>Aging cell</title><addtitle>Aging Cell</addtitle><description>Summary
Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF.</description><subject>Age</subject><subject>Aged</subject><subject>Aging - genetics</subject><subject>Aging - immunology</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>C-Reactive Protein - genetics</subject><subject>C-Reactive Protein - immunology</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - immunology</subject><subject>Frail Elderly</subject><subject>Frailty</subject><subject>Frailty - genetics</subject><subject>Frailty - immunology</subject><subject>Frailty - physiopathology</subject><subject>Gene Expression Regulation - immunology</subject><subject>Gerontology</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - immunology</subject><subject>Heart Failure - pathology</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Inflammation</subject><subject>pathophysiology</subject><subject>Review</subject><subject>Reviews</subject><subject>Sarcopenia</subject><subject>Sarcopenia - genetics</subject><subject>Sarcopenia - immunology</subject><subject>Sarcopenia - pathology</subject><subject>Signal Transduction</subject><subject>Toll-Like Receptors - genetics</subject><subject>Toll-Like Receptors - immunology</subject><issn>1474-9718</issn><issn>1474-9726</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp9kctuEzEUhi0EohfY8ABoJDZVpQTb8W1YgKKoQNVIsIC15fHYiasZO9gzRfP2nJASKELYC9--85_j_yD0guA5gfHaWNfNCeWKPEKnhEk2qyUVj497ok7QWSm3GBNZ48VTdEIVFYIIeYpuPpthm3bbqYTUpc1UJV9tnclD5U3oxuwqE9vKZzgM05vKVDb1fYpViL4zfW-GlCEmh02I756hJ950xT2_X8_R1_dXX1YfZ-tPH65Xy_XMQolkZoVvvcW8JaqhDfWs4ZYQZrExSnBqfO0w5pK3Hkq0omkWRlDHae0FFrJmi3P09qC7G5vetdbFIZtO73LoTZ50MkE_fIlhqzfpTnNGFMUCBC7uBXL6Nroy6D4UMLEz0aWxaKIkJ4xjKgF99Rd6m8Yc4XtA1ZxiplT9m9qYzmnwJkFeuxfVS4mlYgQcB2r-Dwpm6_pgU3Q-wP2DgMtDgM2plOz88Y8E633r9b71-mfrAX75pytH9FevASAH4Dukmf4jpZerq_VB9AePobgD</recordid><startdate>201706</startdate><enddate>201706</enddate><creator>Bellumkonda, Lavanya</creator><creator>Tyrrell, Daniel</creator><creator>Hummel, Scott L.</creator><creator>Goldstein, Daniel R.</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201706</creationdate><title>Pathophysiology of heart failure and frailty: a common inflammatory origin?</title><author>Bellumkonda, Lavanya ; Tyrrell, Daniel ; Hummel, Scott L. ; Goldstein, Daniel R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5811-c6fdfc05d18b2b2f4b5c114c0aa8652af9e00575df616c6bb3a62e529f6067943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Age</topic><topic>Aged</topic><topic>Aging - genetics</topic><topic>Aging - immunology</topic><topic>Aging - pathology</topic><topic>Animals</topic><topic>C-Reactive Protein - genetics</topic><topic>C-Reactive Protein - immunology</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - immunology</topic><topic>Frail Elderly</topic><topic>Frailty</topic><topic>Frailty - genetics</topic><topic>Frailty - immunology</topic><topic>Frailty - physiopathology</topic><topic>Gene Expression Regulation - immunology</topic><topic>Gerontology</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Failure - genetics</topic><topic>Heart Failure - immunology</topic><topic>Heart Failure - pathology</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Inflammation</topic><topic>pathophysiology</topic><topic>Review</topic><topic>Reviews</topic><topic>Sarcopenia</topic><topic>Sarcopenia - genetics</topic><topic>Sarcopenia - immunology</topic><topic>Sarcopenia - pathology</topic><topic>Signal Transduction</topic><topic>Toll-Like Receptors - genetics</topic><topic>Toll-Like Receptors - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bellumkonda, Lavanya</creatorcontrib><creatorcontrib>Tyrrell, Daniel</creatorcontrib><creatorcontrib>Hummel, Scott L.</creatorcontrib><creatorcontrib>Goldstein, Daniel R.</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Aging cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bellumkonda, Lavanya</au><au>Tyrrell, Daniel</au><au>Hummel, Scott L.</au><au>Goldstein, Daniel R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathophysiology of heart failure and frailty: a common inflammatory origin?</atitle><jtitle>Aging cell</jtitle><addtitle>Aging Cell</addtitle><date>2017-06</date><risdate>2017</risdate><volume>16</volume><issue>3</issue><spage>444</spage><epage>450</epage><pages>444-450</pages><issn>1474-9718</issn><eissn>1474-9726</eissn><abstract>Summary
Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>28266167</pmid><doi>10.1111/acel.12581</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Age Aged Aging - genetics Aging - immunology Aging - pathology Animals C-Reactive Protein - genetics C-Reactive Protein - immunology Cytokines Cytokines - genetics Cytokines - immunology Frail Elderly Frailty Frailty - genetics Frailty - immunology Frailty - physiopathology Gene Expression Regulation - immunology Gerontology Heart diseases Heart failure Heart Failure - genetics Heart Failure - immunology Heart Failure - pathology Humans Immunity, Innate Inflammation pathophysiology Review Reviews Sarcopenia Sarcopenia - genetics Sarcopenia - immunology Sarcopenia - pathology Signal Transduction Toll-Like Receptors - genetics Toll-Like Receptors - immunology |
title | Pathophysiology of heart failure and frailty: a common inflammatory origin? |
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