NAD+ supplementation prevents STING-induced senescence in CD8+ T cells by improving mitochondrial homeostasis
© 2024 Wiley Periodicals LLC..
Understanding the connection between senescence phenotypes and mitochondrial dysfunction is crucial in aging and premature aging diseases. Loss of mitochondrial function leads to a decline in T cell function, which plays a significant role in this process. However, more research is required to determine if improving mitochondrial homeostasis alleviates senescence phenotypes. Our research has shown an association between NAD+ and senescent T cells through the cGAS-STING pathway, which can lead to an inflammatory phenotype. Further research is needed to fully understand the role of NAD+ in T-cell aging and how it can be utilized to improve mitochondrial homeostasis and alleviate senescence phenotypes. We demonstrate here that mitochondrial dysfunction and cellular senescence with a senescence-associated secretory phenotype (SASP) occur in senescent T cells and tumor-bearing mice. Senescence is mediated by a stimulator of interferon genes (STING) and involves ectopic cytoplasmic DNA. We further show that boosting intracellular NAD+ levels with nicotinamide mononucleotide (NMN) prevents senescence and SASP by promoting mitophagy. NMN treatment also suppresses senescence and neuroinflammation and improves the survival cycle of mice. Encouraging mitophagy may be a useful strategy to prevent CD8+ T cells from senescence due to mitochondrial dysfunction. Additionally, supplementing with NMN to increase NAD+ levels could enhance survival rates in mice while also reducing senescence and inflammation, and enhancing mitophagy as a potential therapeutic intervention.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:125 |
|---|---|
| Enthalten in: |
Journal of cellular biochemistry - 125(2024), 3 vom: 15. März, Seite e30522 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Ye, Bin [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
0U46U6E8UK |
|---|
| Anmerkungen: |
Date Completed 12.03.2024 Date Revised 12.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1002/jcb.30522 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM367147335 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM367147335 | ||
| 003 | DE-627 | ||
| 005 | 20240312233606.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240115s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1002/jcb.30522 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1324.xml |
| 035 | |a (DE-627)NLM367147335 | ||
| 035 | |a (NLM)38224175 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Ye, Bin |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a NAD+ supplementation prevents STING-induced senescence in CD8+ T cells by improving mitochondrial homeostasis |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 12.03.2024 | ||
| 500 | |a Date Revised 12.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2024 Wiley Periodicals LLC. | ||
| 520 | |a Understanding the connection between senescence phenotypes and mitochondrial dysfunction is crucial in aging and premature aging diseases. Loss of mitochondrial function leads to a decline in T cell function, which plays a significant role in this process. However, more research is required to determine if improving mitochondrial homeostasis alleviates senescence phenotypes. Our research has shown an association between NAD+ and senescent T cells through the cGAS-STING pathway, which can lead to an inflammatory phenotype. Further research is needed to fully understand the role of NAD+ in T-cell aging and how it can be utilized to improve mitochondrial homeostasis and alleviate senescence phenotypes. We demonstrate here that mitochondrial dysfunction and cellular senescence with a senescence-associated secretory phenotype (SASP) occur in senescent T cells and tumor-bearing mice. Senescence is mediated by a stimulator of interferon genes (STING) and involves ectopic cytoplasmic DNA. We further show that boosting intracellular NAD+ levels with nicotinamide mononucleotide (NMN) prevents senescence and SASP by promoting mitophagy. NMN treatment also suppresses senescence and neuroinflammation and improves the survival cycle of mice. Encouraging mitophagy may be a useful strategy to prevent CD8+ T cells from senescence due to mitochondrial dysfunction. Additionally, supplementing with NMN to increase NAD+ levels could enhance survival rates in mice while also reducing senescence and inflammation, and enhancing mitophagy as a potential therapeutic intervention | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a SASP | |
| 650 | 4 | |a cGAS-STING | |
| 650 | 4 | |a mitochondria | |
| 650 | 4 | |a nicotinamide mononucleotide | |
| 650 | 4 | |a senescence | |
| 650 | 7 | |a NAD |2 NLM | |
| 650 | 7 | |a 0U46U6E8UK |2 NLM | |
| 700 | 1 | |a Pei, Yingting |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Lujing |e verfasserin |4 aut | |
| 700 | 1 | |a Meng, Dehao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Zou, Shuang |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Henian |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Jinying |e verfasserin |4 aut | |
| 700 | 1 | |a Xie, Ziying |e verfasserin |4 aut | |
| 700 | 1 | |a Tian, Changhong |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Yuqi |e verfasserin |4 aut | |
| 700 | 1 | |a Qiao, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Xu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Yanfen |e verfasserin |4 aut | |
| 700 | 1 | |a Ma, Ning |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of cellular biochemistry |d 1985 |g 125(2024), 3 vom: 15. März, Seite e30522 |w (DE-627)NLM012621285 |x 1097-4644 |7 nnns |
| 773 | 1 | 8 | |g volume:125 |g year:2024 |g number:3 |g day:15 |g month:03 |g pages:e30522 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1002/jcb.30522 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 125 |j 2024 |e 3 |b 15 |c 03 |h e30522 | ||