lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases
Aging and age-related diseases (ARDs) share basic mechanisms largely involving inflammation. A chronic, low-grade, subclinical inflammation called inflammaging occurs during aging. Autophagy defects, oxidative stresses, senescence-associated secretory phenotypes (SASPs), and DNA damage generally con...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2019-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2019/4260309 |
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| _version_ | 1832545776901816320 |
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| author | Lulingxiao Nie Peng Zhang Qian Wang Xinyi Zhou Qi Wang |
| author_facet | Lulingxiao Nie Peng Zhang Qian Wang Xinyi Zhou Qi Wang |
| author_sort | Lulingxiao Nie |
| collection | DOAJ |
| description | Aging and age-related diseases (ARDs) share basic mechanisms largely involving inflammation. A chronic, low-grade, subclinical inflammation called inflammaging occurs during aging. Autophagy defects, oxidative stresses, senescence-associated secretory phenotypes (SASPs), and DNA damage generally contribute to inflammaging and are largely regulated by numerous lncRNA through two-level vicious cycles disrupting cellular homeostasis: (1) inflammaging and the cellular senescence cascade and (2) autophagy defects, oxidative stress, and the SASP cascade. SASPs and inflammasomes simultaneously cause inflammaging. This review discusses the involvement of macrophage inflammaging in various ARDs and its regulation via lncRNA. Among macrophages, this phenomenon potentially impairs its immunosurveillance and phagocytosis mechanisms, leading to decreased recognition and clearance of malignant and senescent cells. Moreover, SASPs extracellularly manifest to induce paracrine senescence. Macrophage senescence escalates to organ level malfunction, and the organism is more prone to ARDs. By targeting genes and proteins or functioning as competing endogenous RNA (ceRNA), lncRNA regulates different phenomena including inflammaging and ARDs. The detailed mechanism warrants further elucidation to obtain pathological evidence of ARDs and potential treatment approaches. |
| format | Article |
| id | doaj-art-4a57ba5c8fe5466e8bc8f223a7e2eb8d |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4a57ba5c8fe5466e8bc8f223a7e2eb8d2025-02-03T07:24:41ZengWileyMediators of Inflammation0962-93511466-18612019-01-01201910.1155/2019/42603094260309lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related DiseasesLulingxiao Nie0Peng Zhang1Qian Wang2Xinyi Zhou3Qi Wang4State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, ChinaAging and age-related diseases (ARDs) share basic mechanisms largely involving inflammation. A chronic, low-grade, subclinical inflammation called inflammaging occurs during aging. Autophagy defects, oxidative stresses, senescence-associated secretory phenotypes (SASPs), and DNA damage generally contribute to inflammaging and are largely regulated by numerous lncRNA through two-level vicious cycles disrupting cellular homeostasis: (1) inflammaging and the cellular senescence cascade and (2) autophagy defects, oxidative stress, and the SASP cascade. SASPs and inflammasomes simultaneously cause inflammaging. This review discusses the involvement of macrophage inflammaging in various ARDs and its regulation via lncRNA. Among macrophages, this phenomenon potentially impairs its immunosurveillance and phagocytosis mechanisms, leading to decreased recognition and clearance of malignant and senescent cells. Moreover, SASPs extracellularly manifest to induce paracrine senescence. Macrophage senescence escalates to organ level malfunction, and the organism is more prone to ARDs. By targeting genes and proteins or functioning as competing endogenous RNA (ceRNA), lncRNA regulates different phenomena including inflammaging and ARDs. The detailed mechanism warrants further elucidation to obtain pathological evidence of ARDs and potential treatment approaches.http://dx.doi.org/10.1155/2019/4260309 |
| spellingShingle | Lulingxiao Nie Peng Zhang Qian Wang Xinyi Zhou Qi Wang lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases Mediators of Inflammation |
| title | lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases |
| title_full | lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases |
| title_fullStr | lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases |
| title_full_unstemmed | lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases |
| title_short | lncRNA-Triggered Macrophage Inflammaging Deteriorates Age-Related Diseases |
| title_sort | lncrna triggered macrophage inflammaging deteriorates age related diseases |
| url | http://dx.doi.org/10.1155/2019/4260309 |
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