Article
Oncology
Seon Mee Kang, Hye Sook Jung, Min Jeong Kwon, Soon Hee Lee, Jeong Hyun Park
Summary: The DPP-4 inhibitor anagliptin was found to protect vascular endothelial cells from stress-induced accelerated senescence, reducing markers of aging and alleviating cellular stress responses.
ANNALS OF TRANSLATIONAL MEDICINE
(2021)
Article
Environmental Sciences
Yiqi Fu, Mengqi Fan, Liwang Xu, Hui Wang, Qinglian Hu, Yuanxiang Jin
Summary: Nano-plastics, as emerging contaminants, have adverse effects on the ecosystem and human health. This study investigated the biological effects of noncharged polystyrene nano-plastics and amino-functionalized nano-plastics on human umbilical vein endothelial cells. The results showed that the amino-functionalized nano-plastics had higher cytotoxicity and dysregulated mitochondrial function in endothelial cells.
Article
Geriatrics & Gerontology
Chiara Grasselli, Silvia Bombelli, Stefano Eriani, Giulia Domenici, Riccardo Galluccio, Chiara Tropeano, Sofia De Marco, Maddalena M. Bolognesi, Barbara Torsello, Cristina Bianchi, Laura Antolini, Fabio Rossi, Paolo Mazzola, Valerio Leoni, Giuseppe Bellelli, Roberto A. Perego
Summary: Frailty is an age-related syndrome that increases vulnerability and often leads to negative outcomes, including mortality. The mechanisms behind frailty are still unclear, but oxidative stress and DNA damage are believed to play a significant role. Early diagnosis and targeted treatments could potentially slow down the progression of frailty.
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
(2022)
Review
Geriatrics & Gerontology
Shital Wakale, Xiaoxin Wu, Yogita Sonar, Antonia Sun, Xiwei Fan, Ross Crawford, Indira Prasadam
Summary: Osteoarthritis (OA) is a common degenerative joint disease that significantly impairs the physical function of the elderly population. This review focuses on the age-related changes in chondrocytes and their impact on OA development, including senescence, mitochondrial dysfunction, epigenetic modifications, and decreased growth factor response. These changes also extend to the matrix, subchondral bone, and synovium. Understanding these alterations provides potential therapeutic approaches for OA treatment.
Article
Biochemistry & Molecular Biology
Boying Zhao, Jiang Yu, Yuan Luo, Ming Xie, Can Qu, Qiong Shi, Xiaowen Wang, Xingji Zhao, Lingwen Kong, Yu Zhao, Yongzheng Guo
Summary: S100A9 plays a crucial role in the inflammatory response and contributes to aging-related pathologies and endothelial dysfunction. The deficiency of S100A9 alleviates vascular senescence, improves insulin resistance, reduces oxidative stress and inflammation in aged mice. The study suggests that targeting the S100A9/TLR4 signaling pathway may be a potential therapeutic strategy to prevent age-related cardiovascular diseases.
Article
Toxicology
T. Nakajo, N. Kitajima, T. Katayoshi, K. Tsuji-Naito
Summary: This study demonstrated that nicotinamide mononucleotide (NMN) inhibits oxidative stress-induced damage by activating the sirtuin 1 (SIRT1)/NAD(P)H: quinone oxidoreductase 1 (NQO-1) axis in human umbilical vein endothelial cells (HUVECs). NMN prevented cytotoxicity and senescence-associated protein expression induced by H2O2, as well as actin cytoskeletal disorganization, by inhibiting reactive oxygen species (ROS) production. NMN-inducible NQO-1 was associated with SIRT1 activity, and inhibition of SIRT1 and NQO-1 attenuated the protective effects of NMN against H2O2-induced damage.
TOXICOLOGY IN VITRO
(2023)
Article
Cell Biology
Md Torikul Islam, Shelby A. Hall, Tavia Dutson, Samuel I. Bloom, R. Colton Bramwell, John Kim, Jordan R. Tucker, Daniel R. Machin, Anthony J. Donato, Lisa A. Lesniewski
Summary: Inhibition of mTOR can delay aging and improve age-related conditions, but the specific mechanisms and tissues involved are unclear. This study found that activation of mTOR in endothelial cells is associated with arterial and metabolic dysfunction. Reducing endothelial mTOR can reverse arterial stiffening, improve arterial and metabolic function, and reduce senescence, inflammation, and oxidative stress in arteries, lungs, adipose tissue, and liver.
Article
Neurosciences
Rezwana Ahmed, Yasukazu Nakahata, Kazuyuki Shinohara, Yasumasa Bessho
Summary: Cellular senescence, whether replicative or stress-induced premature, triggers altered circadian clock properties, including prolonged period and delayed phases. Oxidative stress induces changes in the circadian clock of senescent cells, intensifying over time. This study confirms that cellular senescence affects circadian clock properties, regardless of the type of senescence.
FRONTIERS IN NEUROSCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Guan Wang, Mingyue Hao, Qiong Liu, Yanlong Jiang, Haibin Huang, Guilian Yang, Chunfeng Wang
Summary: The study found that NC8-pSIP409-alr-ACEIP has a protective effect against H2O2-induced cell death in HUVEC cells, reducing apoptosis rate and levels of oxidative stress indicators such as iNOS, gp91phox, MDA, and ROS, while increasing SOD expression to enhance antioxidant capacity.
JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B
(2021)
Review
Endocrinology & Metabolism
Wenqian Zhang, Yuan Xiong, Ranyang Tao, Adriana C. Panayi, Bobin Mi, Guohui Liu
Summary: This review outlines the connection between cell senescence and the clock gene BMAL1, highlighting the potential therapeutic target that regulating the cell senescence process may offer in handling aging-associated diseases.
FRONTIERS IN ENDOCRINOLOGY
(2022)
Article
Biology
Diptiman Chanda, Mohammad Rehan, Samuel R. Smith, Kevin G. Dsouza, Yong Wang, Karen Bernard, Deepali Kurundkar, Vinayak Memula, Kyoko Kojima, James A. Mobley, Gloria A. Benavides, Victor Darley-Usmar, Young-iL Kim, Jaroslaw W. Zmijewski, Jessy S. Deshane, Stijn De Langhe, Victor J. Thannickal
Summary: This study revealed the impact of cellular aging on the ability of L-MSC and AEC2s cells to form three-dimensional organoids, and found that reducing Nox4 activity may reverse critical effects of cellular aging.
Article
Biochemistry & Molecular Biology
Emilio Sosa-Diaz, Estefani Yaquelin Hernandez-Cruz, Jose Pedraza-Chaverri
Summary: Vitamin D is considered essential for human health and plays a crucial role in delaying cellular senescence and attenuating oxidative stress, making it a promising candidate for preventing age-related diseases. However, further research is needed to fully understand the mechanisms behind its effects.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Fanglin Niu, Zhuozhuo Li, Yuanyuan Ren, Zi Li, Hua Guan, Yang Li, Yan Zhang, Yirong Li, Junle Yang, Lu Qian, Wenzhen Shi, Xiaobin Fan, Jinli Li, Lele Shi, Yi Yu, Yuyan Xiong
Summary: This study found that abnormal hyperexpression of GIGYF2 was observed in senescent human endothelial cells (ECs) and the aortas of old mice. Silencing GIGYF2 can suppress the senescence and dysfunction of ECs. On the contrary, overexpression of GIGYF2 promotes senescence, dysfunction, and activation of the mTORC1-SK61 pathway in non-senescent cells. The study also revealed that GIGYF2 acts as an RNA binding protein (RBP) to enhance STAU1 mRNA stability and that LAMTOR4 expression is upregulated by the binding of STAU1 protein to its intron region. The disruption of the GIGYF2-STAU1-mTORC1 signaling cascade may be a promising therapeutic approach against vascular aging and aging-related cardiovascular diseases.
Article
Cell Biology
Sunny Shinchen Lee, Thu Thuy Vu, Anthony S. Weiss, Giselle C. Yeo
Summary: Mesenchymal stem cells (MSCs) hold promise as cell-based therapies for degenerative and inflammatory conditions. However, their clinical translation is hindered by the heterogeneity and senescence of MSC populations, leading to inconsistent therapeutic efficacy. This review discusses the regenerative properties of MSCs, the triggers and mechanisms of MSC senescence, and strategies to delay or rejuvenate functions lost to senescence.
EUROPEAN JOURNAL OF CELL BIOLOGY
(2023)
Article
Cell Biology
Yoon Seon Lee, Yeoung-Hyun Park, Geumbit Hwang, Hyejin Seo, Si Hyoung Ki, Shengfeng Bai, Chul Son, Seong Min Roh, Su-Jin Park, Dong-Seol Lee, Ji-Hyun Lee, You-Mi Seo, Won Jun Shon, Daehyun Jeon, Mi Jang, Sahng G. Kim, Byoung-Moo Seo, Gene Lee, Joo-Cheol Park
Summary: Loss of Cpne7 accelerates cellular senescence in odontoblasts due to oxidative stress and DNA damage accumulation, leading to impaired survival and aberrant dentin formation. However, treatment with CPNE7-derived functional peptide or Cpne7 transgenic mice rescue the aged dental pulp phenotype.
