A single-cell transcriptomic atlas of exercise-induced anti-inflammatory and geroprotective effects across the body

Sun, Shuhui; Ma, Shuai; Cai, Yusheng; Wang, Si; Ren, Jie; Yang, Yuan‐Han; Ping, Jiale; Wang, Xuebao; Zhang, Yiyuan; Yan, Haoteng; Li, Wei; Esteban, Concepción Rodrı́guez; Yu, Yan; Liu, Feifei; Belmonte, Juan Carlos Izpisúa; Zhang, Weiqi; Qu, Jing; Liu, Guanghui

doi:10.1016/j.xinn.2023.100380

Cited by 19 publications

(22 citation statements)

References 81 publications

(89 reference statements)

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“…Tony Wyss-Coray group found that the blood produced anti-inflammatory factors as well as complement signal inhibitory factors such as Clusterin (CLU), factor H (FH), glycoprotein pigment epithelium-derived factor (PEDF), and leukemia inhibitory factor receptor (LIFE), all increase their levels in the plasma after exercise (De Miguel et al, 2021), which could be beneficial against brain aging. And the effect of long-term exercise on the brain itself is demonstrated by another study as evidenced by the increased thickness of the cortex and reduced inflammation in the entire CNS in aged mice (Sun et al, 2023).…”

Section: Secretory Factors Detectable In Biofluidsmentioning

confidence: 87%

“…BMAL1 and CLOCK facilitate heterochromatin stabilization and prevent the senescence of mesenchymal stem cells (Liang et al, 2022;Liang et al, 2021). A recent study reveals that exercise can restore dysregulated circadian machinery in different cell types across tissues in aged mice (Sun et al, 2023). Particularly, the transcription of Bmal1 is downregulated in various endothelial cells during aging, which was rescued by prolonged exercise, while overexpression of Bmal1 delays the senescence of cardiac endothelial cells.…”

Section: Circadian Clocksmentioning

confidence: 99%

“…Changes in RNA expression levels both in single cells or bulk tissues during aging have been widely reported in various common model organisms across tissues, and a large number of data resources and databases have been developed (Aging Atlas, 2021;Kang et al, 2022;Ma et al, 2020;Sun et al, 2023;Tabula Muris, 2020;Yan et al, 2023). The association between genes with aging makes it possible to predict the rate of aging or lifespan based on transcriptome data.…”

Section: Aging Clocks Based On Single-cell Transcriptomementioning

confidence: 99%

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Biomarkers of aging

Bao

Cao

Chen

et al. 2023

Sci. China Life Sci.

117

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Aging biomarkers are a combination of biological parameters to (i) assess age-related changes, (ii) track the physiological aging process, and (iii) predict the transition into a pathological status. Although a broad spectrum of aging biomarkers has been developed, their potential uses and limitations remain poorly characterized. An immediate goal of biomarkers is to help us answer the following three fundamental questions in aging research: How old are we? Why do we get old? And how can we age slower? This review aims to address this need. Here, we summarize our current knowledge of biomarkers developed for cellular, organ, and organismal levels of aging, comprising six pillars: physiological characteristics, medical imaging, histological features, cellular alterations, molecular changes, and secretory factors. To fulfill all these requisites, we propose that aging biomarkers should qualify for being specific, systemic, and clinically relevant. Supporting Information The supporting information is available online at 10.1007/s11427-023-2305-0. The supporting materials are published as submitted, without typesetting or editing. The responsibility for scientific accuracy and content remains entirely with the authors.

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Section: Secretory Factors Detectable In Biofluidsmentioning

confidence: 87%

Section: Circadian Clocksmentioning

confidence: 99%

Section: Aging Clocks Based On Single-cell Transcriptomementioning

confidence: 99%

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Biomarkers of aging

Bao

Cao

Chen

et al. 2023

Sci. China Life Sci.

117

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“…It has been reported that exercise training provides beneficial effects in various liver diseases, including hepatic ischemia-reperfusion injury [ 18 ], drug-related liver injury [ 19 ], and non-alcoholic fatty liver disease (NAFLD) [ 20 ]. The mechanisms were related to inhibiting ROS and inflammation, regulating M1/M2 macrophages polarization, increasing β-oxidation and reducing intrahepatic fat content, hepatocyte autophagy, and apoptosis [ 18 , 21 , 22 , 23 , 24 ]. It has been demonstrated that aerobic exercise (AE) ameliorated liver injury in MI rats by reducing oxidative stress [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

FNDC5/Irisin Inhibits the Inflammatory Response and Mediates the Aerobic Exercise-Induced Improvement of Liver Injury after Myocardial Infarction

Wang

et al. 2023

IJMS

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Myocardial infarction (MI) causes peripheral organ injury, in addition to cardiac dysfunction, including in the liver, which is known as cardiac hepatopathy. Aerobic exercise (AE) can effectively improve liver injury, although the mechanism and targets are currently not well established. Irisin, mainly produced by cleavage of the fibronectin type III domain-containing protein 5 (FNDC5), is a responsible for the beneficial effects of exercise training. In this study, we detected the effect of AE on MI-induced liver injury and explored the role of irisin alongside the benefits of AE. Wildtype and Fndc5 knockout mice were used to establish an MI model and subjected to AE intervention. Primary mouse hepatocytes were treated with lipopolysaccharide (LPS), rhirisin, and a phosphoinositide 3-kinase (PI3K) inhibitor. The results showed that AE significantly promoted M2 polarization of macrophages and improved MI-induced inflammation, upregulated endogenous irisin protein expression and activated the PI3K/ protein kinase B (Akt) signaling pathway in the liver of MI mice, while knockout of Fndc5 attenuated the beneficial effects of AE. Exogenous rhirisin significantly inhibited the LPS-induced inflammatory response, which was attenuated by the PI3K inhibitor. These results suggest that AE could effectively activate the FNDC5/irisin-PI3K/Akt signaling pathway, promote the polarization of M2 macrophages, and inhibit the inflammatory response of the liver after MI.

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“…Forelimb and hind limb grip strength was measured using a grip strength meter (Panlab Grid Strength Meter, LE902) as previously reported. 21,22 Briefly, mice in Sham, post-injury-Vehicle and postinjury-rSESN1 groups were held by the tail and allowed to hold the grid of the apparatus. Mice were gently pulled away from the grid until they released the grid.…”

Section: Grip Strength Testmentioning

confidence: 99%

SESN1 is a FOXO3 effector that counteracts human skeletal muscle ageing

et al. 2023

Self Cite

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Sarcopenia, a skeletal muscle disorder in which loss of muscle mass and function progresses with age, is associated with increased overall frailty, risk of falling and mortality in the elders. Here, we reveal that SESN1 safeguards skeletal muscle from ageing downstream of the longevity gene FOXO3, which we recently reported is a geroprotector in primate skeletal muscle. Knockdown of SESN1 mimicked the human myotube ageing Ying Jing, Yuesheng Zuo, Liang Sun and Zheng-Rong Yu contributed equally to this study.

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A single-cell transcriptomic atlas of exercise-induced anti-inflammatory and geroprotective effects across the body

Cited by 19 publications

References 81 publications

Biomarkers of aging

Biomarkers of aging

FNDC5/Irisin Inhibits the Inflammatory Response and Mediates the Aerobic Exercise-Induced Improvement of Liver Injury after Myocardial Infarction

SESN1 is a FOXO3 effector that counteracts human skeletal muscle ageing

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