The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Hydrogen Sulfide Protects Against Cellular Senescence via S -Sulfhydration of Keap1 and Activation of Nrf2
Abstract
AIMS: H2S, a third member of gasotransmitter family along with nitric oxide and carbon monoxide, exerts a wide range of cellular and molecular actions in our body. Cystathionine gamma-lyase (CSE) is a major H2S-generating enzyme in our body. Aging at the cellular level, known as cellular senescence, can result from increases in oxidative stress. The aim of this study was to investigate how H2S attenuates oxidative stress and delays cellular senescence. RESULTS: Here we showed that mouse embryonic fibroblasts isolated from CSE knockout mice (CSE KO-MEFs) display increased oxidative stress and accelerated cellular senescence in comparison with MEFs from wild-type mice (WT-MEFs). The protein expression of p53 and p21 was significantly increased in KO-MEFs, and knockdown of p53 or p21 reversed CSE deficiency-induced senescence. Incubation of the cells with NaHS (a H2S donor) significantly increased the glutathione (GSH) level and rescued KO-MEFs from senescence. Nrf2 is a master regulator of the antioxidant response, and Keap1 acts as a negative regulator of Nrf2. NaHS S-sulfhydrated Keap1 at cysteine-151, induced Nrf2 dissociation from Keap1, enhanced Nrf2 nuclear translocation, and stimulated mRNA expression of Nrf2-targeted downstream genes, such as glutamate-cysteine ligase and GSH reductase. INNOVATION: These results provide a mechanistic insight into how H2S signaling mediates cellular senescence induced by oxidative stress. CONCLUSION: H2S protects against cellular aging via S-sulfhydration of Keap1 and Nrf2 activation in association with oxidative stress.
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Cites
H 2 S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
Yang, G., Wu, L., Jiang, B., Yang, W., Qi, J., Cao, K., Meng, Q., Mustafa, A. K., Mu, W., Zhang, S., et al. (2008) · Science · doi:10.1126/science.1162667 · Cited by 2,310
Self-citationDinkova-Kostova, A. T., Holtzclaw, W. D., Cole, R. N., Itoh, K., Wakabayashi, N., Katoh, Y., Yamamoto, M., & Talalay, P. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.172398899 · Cited by 1,947
Zhang, D. D., & Hannink, M. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.22.8137-8151.2003 · Cited by 1,480 · cited 5×
“The second is located at cysteine-151 in the BTB domain (17, 44).”
InfluentialThe signals and pathways activating cellular senescence
Ben-Porath, I., & Weinberg, R. A. (2005) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2004.10.013 · Cited by 1,046
Feedback between p21 and reactive oxygen production is necessary for cell senescence
Passos, J. F., Nelson, G., Wang, C., Richter, T., Simillion, C., Proctor, C. J., Miwa, S., Olijslagers, S., Hallinan, J., Wipat, A., et al. (2010) · Molecular Systems Biology · doi:10.1038/msb.2010.5 · Cited by 1,019 · cited 3×
“Several paradigmatic tumor suppressor proteins, p53, p21 and p16, are the central activating pathway of senescence (1, 29).”
Integrated Stress Response Modulates Cellular Redox State via Induction of Cystathionine γ-Lyase
Dickhout, J. G., Carlisle, R. E., Jerome, D. E., Mohammed-Ali, Z., Jiang, H., Yang, G., Mani, S., Garg, S. K., Banerjee, R., Kaufman, R. J., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.304576 · Cited by 129
Self-citationEarly onset senescence occurs when fibroblasts lack the glutamate–cysteine ligase modifier subunit
Chen, Y., Johansson, E., Fan, Y., Shertzer, H. G., Vasiliou, V., Nebert, D. W., & Dalton, T. P. (2009) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.05.003 · Cited by 28
Cited by
The Molecular Mechanisms Regulating the KEAP1-NRF2 Pathway
Baird, L., & Yamamoto, M. (2020) · Molecular and Cellular Biology · doi:10.1128/mcb.00099-20 · Cited by 1,542
Chemical Biology of H2S Signaling through Persulfidation
Filipovic, M. R., Zivanovic, J., Alvarez, B., & Banerjee, R. (2018) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00205 · Cited by 1,046
Toward clinical application of the Keap1-Nrf2 pathway
Suzuki, T., Motohashi, H., & Yamamoto, M. (2013) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2013.04.005 · Cited by 680
Physiological roles of hydrogen sulfide in mammalian cells, tissues, and organs
Cirino, G., Szabo, C., & Papapetropoulos, A. (2023) · Physiological Reviews · doi:10.1152/physrev.00028.2021 · Cited by 553
Pedre, B., Barayeu, U., Ezeriņa, D., & Dick, T. P. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2021.107916 · Cited by 470
Metadata
- Authors
- Yang, G., Zhao, K., Ju, Y., Mani, S., Cao, Q., Puukila, S., Khaper, N., Wu, L., & Wang, R.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2013-05-20
- Volume
- 18
- Issue
- 15
- Pages
- 1906-1919
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W2006242918
- Cited by
- 563
- References
- 7
- FWCI
- 11.97
- Type
- journal article
- Language
- en
- Open access
- closed
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- Yang, G., Zhao, K., Ju, Y., Mani, S., Cao, Q., Puukila, S., Khaper, N., Wu, L., & Wang, R. (2013). Hydrogen Sulfide Protects Against Cellular Senescence via S -Sulfhydration of Keap1 and Activation of Nrf2. Antioxidants & Redox Signaling. https://doi.org/10.1089/ars.2012.4645
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