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Senoinflammation: A major mediator underlying age-related metabolic dysregulation
Chronic inflammation is a complex and unresolved inflammatory response with low-grade multivariable patterns that aggravate systemic pathophysiological conditions and the aging process. To redefine and delineate these age-related complex inflammatory phenomena at the molecular, cellular, and systemi...
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Published in: | Experimental gerontology 2020-06, Vol.134, p.110891-110891, Article 110891 |
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container_title | Experimental gerontology |
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creator | Kim, Dae Hyun Bang, EunJin Arulkumar, Radha Ha, Sugyeong Chung, Ki Wung Park, Min Hi Choi, Yeon Ja Yu, Byung Pal Chung, Hae Young |
description | Chronic inflammation is a complex and unresolved inflammatory response with low-grade multivariable patterns that aggravate systemic pathophysiological conditions and the aging process. To redefine and delineate these age-related complex inflammatory phenomena at the molecular, cellular, and systemic levels, the concept of “Senoinflammation” was recently formulated.
In this review, we describe the accumulated data on both the multiphase systemic inflammatory process and the cellular proinflammatory signaling pathway. We also describe the proinflammatory mechanisms underlying the metabolic molecular pathways in aging. Additionally, we review age-related lipid accumulation, the role of the inflammatory senescence-associated secretory phenotype (SASP), the involvement of cytokine/chemokine secretion, endoplasmic reticulum (ER) stress, insulin resistance, and autophagy.
The last section of the review highlights the modulation of the senoinflammatory process by the anti-aging and anti-inflammatory action of calorie restriction (CR). Evidence from aging and CR research strongly suggests that SASP from senescent cells may be the major source of secreted cytokines and chemokines during aging. A better understanding of the mechanisms underpinning the senoinflammatory response and the mitigating role of CR will provide insights into the molecular mechanisms of chronic inflammation and aging for potential interventions.
•Transcription factors (NF-κB, FoxOs, SIRT1, and PPARs) are involved in metabolic process.•SASP leading to various metabolic disorders and relevant pathological symptoms such as insulin resistance, lipid accumulation, and vicious chronic inflammation.•Anti-aging effects of CR modulates insulin resistance, hyperinsulemia, and Akt/IKK signaling pathway. |
doi_str_mv | 10.1016/j.exger.2020.110891 |
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In this review, we describe the accumulated data on both the multiphase systemic inflammatory process and the cellular proinflammatory signaling pathway. We also describe the proinflammatory mechanisms underlying the metabolic molecular pathways in aging. Additionally, we review age-related lipid accumulation, the role of the inflammatory senescence-associated secretory phenotype (SASP), the involvement of cytokine/chemokine secretion, endoplasmic reticulum (ER) stress, insulin resistance, and autophagy.
The last section of the review highlights the modulation of the senoinflammatory process by the anti-aging and anti-inflammatory action of calorie restriction (CR). Evidence from aging and CR research strongly suggests that SASP from senescent cells may be the major source of secreted cytokines and chemokines during aging. A better understanding of the mechanisms underpinning the senoinflammatory response and the mitigating role of CR will provide insights into the molecular mechanisms of chronic inflammation and aging for potential interventions.
•Transcription factors (NF-κB, FoxOs, SIRT1, and PPARs) are involved in metabolic process.•SASP leading to various metabolic disorders and relevant pathological symptoms such as insulin resistance, lipid accumulation, and vicious chronic inflammation.•Anti-aging effects of CR modulates insulin resistance, hyperinsulemia, and Akt/IKK signaling pathway.</description><identifier>ISSN: 0531-5565</identifier><identifier>EISSN: 1873-6815</identifier><identifier>DOI: 10.1016/j.exger.2020.110891</identifier><identifier>PMID: 32114077</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Aging ; Calorie restriction ; Chemokines ; Cytokines ; Senoinflammation</subject><ispartof>Experimental gerontology, 2020-06, Vol.134, p.110891-110891, Article 110891</ispartof><rights>2020</rights><rights>Copyright © 2020. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-cab1091046a411ba2ea5b856eeb788739cf8bd556498d2ff1d917f16949b39b43</citedby><cites>FETCH-LOGICAL-c359t-cab1091046a411ba2ea5b856eeb788739cf8bd556498d2ff1d917f16949b39b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S053155651930796X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3536,27905,27906,45761</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32114077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Dae Hyun</creatorcontrib><creatorcontrib>Bang, EunJin</creatorcontrib><creatorcontrib>Arulkumar, Radha</creatorcontrib><creatorcontrib>Ha, Sugyeong</creatorcontrib><creatorcontrib>Chung, Ki Wung</creatorcontrib><creatorcontrib>Park, Min Hi</creatorcontrib><creatorcontrib>Choi, Yeon Ja</creatorcontrib><creatorcontrib>Yu, Byung Pal</creatorcontrib><creatorcontrib>Chung, Hae Young</creatorcontrib><title>Senoinflammation: A major mediator underlying age-related metabolic dysregulation</title><title>Experimental gerontology</title><addtitle>Exp Gerontol</addtitle><description>Chronic inflammation is a complex and unresolved inflammatory response with low-grade multivariable patterns that aggravate systemic pathophysiological conditions and the aging process. To redefine and delineate these age-related complex inflammatory phenomena at the molecular, cellular, and systemic levels, the concept of “Senoinflammation” was recently formulated.
In this review, we describe the accumulated data on both the multiphase systemic inflammatory process and the cellular proinflammatory signaling pathway. We also describe the proinflammatory mechanisms underlying the metabolic molecular pathways in aging. Additionally, we review age-related lipid accumulation, the role of the inflammatory senescence-associated secretory phenotype (SASP), the involvement of cytokine/chemokine secretion, endoplasmic reticulum (ER) stress, insulin resistance, and autophagy.
The last section of the review highlights the modulation of the senoinflammatory process by the anti-aging and anti-inflammatory action of calorie restriction (CR). Evidence from aging and CR research strongly suggests that SASP from senescent cells may be the major source of secreted cytokines and chemokines during aging. A better understanding of the mechanisms underpinning the senoinflammatory response and the mitigating role of CR will provide insights into the molecular mechanisms of chronic inflammation and aging for potential interventions.
•Transcription factors (NF-κB, FoxOs, SIRT1, and PPARs) are involved in metabolic process.•SASP leading to various metabolic disorders and relevant pathological symptoms such as insulin resistance, lipid accumulation, and vicious chronic inflammation.•Anti-aging effects of CR modulates insulin resistance, hyperinsulemia, and Akt/IKK signaling pathway.</description><subject>Aging</subject><subject>Calorie restriction</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Senoinflammation</subject><issn>0531-5565</issn><issn>1873-6815</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kMlOwzAQhi0EoqXwBEgoRy4pnjhxYiQOVcUmVUIIOFu2M6lcZSl2gujb4y5w5DSjmf-f5SPkEugUKPCb1RS_l-imCU1CBWgh4IiMochZzAvIjsmYZgziLOPZiJx5v6KU8oTBKRmxBCCleT4mr2_YdratatU0qrddexvNokatOhc1WFrVh2RoS3T1xrbLSC0xdlirHsvQ75XuamuicuMdLod6N-CcnFSq9nhxiBPy8XD_Pn-KFy-Pz_PZIjYsE31slAYqgKZcpQBaJagyXWQcUedF-EGYqtBlOD4VRZlUFZQC8gq4SIVmQqdsQq73c9eu-xzQ97Kx3mBdqxa7wcuEcVHkPGU8SNlealznw6mVXDvbKLeRQOWWpVzJHUu5ZSn3LIPr6rBg0IHFn-cXXhDc7QUY3vyywe6NxdYEbg5NL8vO_rvgB9JshrA</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Kim, Dae Hyun</creator><creator>Bang, EunJin</creator><creator>Arulkumar, Radha</creator><creator>Ha, Sugyeong</creator><creator>Chung, Ki Wung</creator><creator>Park, Min Hi</creator><creator>Choi, Yeon Ja</creator><creator>Yu, Byung Pal</creator><creator>Chung, Hae Young</creator><general>Elsevier Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20200601</creationdate><title>Senoinflammation: A major mediator underlying age-related metabolic dysregulation</title><author>Kim, Dae Hyun ; Bang, EunJin ; Arulkumar, Radha ; Ha, Sugyeong ; Chung, Ki Wung ; Park, Min Hi ; Choi, Yeon Ja ; Yu, Byung Pal ; Chung, Hae Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-cab1091046a411ba2ea5b856eeb788739cf8bd556498d2ff1d917f16949b39b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Calorie restriction</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Senoinflammation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Dae Hyun</creatorcontrib><creatorcontrib>Bang, EunJin</creatorcontrib><creatorcontrib>Arulkumar, Radha</creatorcontrib><creatorcontrib>Ha, Sugyeong</creatorcontrib><creatorcontrib>Chung, Ki Wung</creatorcontrib><creatorcontrib>Park, Min Hi</creatorcontrib><creatorcontrib>Choi, Yeon Ja</creatorcontrib><creatorcontrib>Yu, Byung Pal</creatorcontrib><creatorcontrib>Chung, Hae Young</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental gerontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Dae Hyun</au><au>Bang, EunJin</au><au>Arulkumar, Radha</au><au>Ha, Sugyeong</au><au>Chung, Ki Wung</au><au>Park, Min Hi</au><au>Choi, Yeon Ja</au><au>Yu, Byung Pal</au><au>Chung, Hae Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Senoinflammation: A major mediator underlying age-related metabolic dysregulation</atitle><jtitle>Experimental gerontology</jtitle><addtitle>Exp Gerontol</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>134</volume><spage>110891</spage><epage>110891</epage><pages>110891-110891</pages><artnum>110891</artnum><issn>0531-5565</issn><eissn>1873-6815</eissn><abstract>Chronic inflammation is a complex and unresolved inflammatory response with low-grade multivariable patterns that aggravate systemic pathophysiological conditions and the aging process. To redefine and delineate these age-related complex inflammatory phenomena at the molecular, cellular, and systemic levels, the concept of “Senoinflammation” was recently formulated.
In this review, we describe the accumulated data on both the multiphase systemic inflammatory process and the cellular proinflammatory signaling pathway. We also describe the proinflammatory mechanisms underlying the metabolic molecular pathways in aging. Additionally, we review age-related lipid accumulation, the role of the inflammatory senescence-associated secretory phenotype (SASP), the involvement of cytokine/chemokine secretion, endoplasmic reticulum (ER) stress, insulin resistance, and autophagy.
The last section of the review highlights the modulation of the senoinflammatory process by the anti-aging and anti-inflammatory action of calorie restriction (CR). Evidence from aging and CR research strongly suggests that SASP from senescent cells may be the major source of secreted cytokines and chemokines during aging. A better understanding of the mechanisms underpinning the senoinflammatory response and the mitigating role of CR will provide insights into the molecular mechanisms of chronic inflammation and aging for potential interventions.
•Transcription factors (NF-κB, FoxOs, SIRT1, and PPARs) are involved in metabolic process.•SASP leading to various metabolic disorders and relevant pathological symptoms such as insulin resistance, lipid accumulation, and vicious chronic inflammation.•Anti-aging effects of CR modulates insulin resistance, hyperinsulemia, and Akt/IKK signaling pathway.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>32114077</pmid><doi>10.1016/j.exger.2020.110891</doi><tpages>1</tpages></addata></record> |
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subjects | Aging Calorie restriction Chemokines Cytokines Senoinflammation |
title | Senoinflammation: A major mediator underlying age-related metabolic dysregulation |
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