Article
Immunology
Yi Xiao, Li Zhang, Xinting Zhu, Ying Qin, Changyan Yu, Nian Jiang, Sanhua Li, Fang Liu, Yun Liu
Summary: The DAF-2/DAF-16 insulin-like signaling pathway regulates various aspects of organismal physiology and is conserved throughout evolution. Luteolin, a flavone found in many plants and vegetables, has been shown to have anti-tumor, antioxidant, and neuroprotective effects. This study found that luteolin increased resistance to both Gram-negative and Gram-positive pathogens in a dose-dependent manner and promoted host immune response. Furthermore, it was discovered that luteolin activated the DAF-16/FOXO transcription factor and promoted innate immunity through the DAF-2/DAF-16 insulin-like signaling pathway.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Cell Biology
Huihui Ji, Zhimin Qi, Daniel Schrapel, Monika Le, Yiqiao Luo, Bin Yan, Jury Gladkich, Michael Schaefer, Li Liu, Ingrid Herr
Summary: Sulforaphane can prolong lifespan and healthspan by inducing the expression and nuclear translocation of TRA-1/GLI, and thus support healthy aging by regulating daf-16/FOXO. However, the prolonging effects of sulforaphane on lifespan and healthspan are inhibited when TRA-1 or daf-16 is interfered with by RNA interference or using worms with mutants of tra-1 or daf-16 genes.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Cell Biology
Zhimin Qi, Huihui Ji, Monika Le, Hanmei Li, Angela Wieland, Sonja Bauer, Li Liu, Michael Wink, Ingrid Herr
Summary: Sulforaphane extends the lifespan of C. elegans by modulating the insulin/IGF-1 signaling pathway, promoting healthspan by increasing mobility and appetite while reducing lipofuscin accumulation.
Article
Biochemistry & Molecular Biology
Juliane C. Campos, Ziyun Wu, Paige D. Rudich, Sonja K. Soo, Meeta Mistry, Julio C. b Ferreira, T. Keith Blackwell, Jeremy M. Van Raamsdonk
Summary: Disrupting subunits of the mitochondrial electron transport chain results in the upregulation of genes involved in innate immunity, which promotes increased resistance to bacterial pathogens and extended longevity in long-lived mitochondrial mutants. Both the p38-mediated innate immune signaling pathway and the mitoUPR act together on the same innate immunity genes to modulate lifespan.
Article
Biology
Richard Venz, Tina Pekec, Iskra Katic, Rafal Ciosk, Collin Yves Ewald
Summary: Geroscience aims to promote health during old age and increase lifespan. By genetically engineering worms to trigger the degradation of the insulin/IGF-1 receptor, researchers were able to double the lifespan of the worms, even at the end of their life span.
Article
Cell Biology
Sonja K. Soo, Annika Traa, Zenith D. Rudich, Alibek Moldakozhayev, Meeta Mistry, Jeremy M. Van Raamsdonk
Summary: Mutations that extend lifespan are associated with enhanced resistance to stress. The study found a strong correlation between stress resistance and longevity, with long-lived mutants showing increased resistance to various stresses. Gene expression analysis revealed the upregulation of multiple stress response pathways in these mutants. Interestingly, there was significant overlap between genes highly correlated with stress resistance and longevity, suggesting the same genetic pathways drive both phenotypes. Disruption of the innate immune signaling pathway showed that it is required for lifespan extension in most mutants.
Article
Biochemistry & Molecular Biology
Xiang Xiao, Yurong Zhou, Cui Tan, Juan Bai, Ying Zhu, Jiayan Zhang, Xinghua Zhou, Yansheng Zhao
Summary: Barley beta-glucan shows potential in defending oxidative stress in C. elegans by reducing ROS levels, enhancing SOD and CAT enzyme activity, decreasing MDA content, and extending lifespan. It participates in anti-oxidative stress partially through the daf-2/daf-16 pathway.
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
(2021)
Review
Genetics & Heredity
Katerina K. Yamamoto, Cathy Savage-Dunn
Summary: This article summarizes the roles of transforming growth factor-beta (TGF-beta) signaling in aging and immunity, highlighting the significance of using Caenorhabditis elegans as a research model.
FRONTIERS IN GENETICS
(2023)
Article
Pharmacology & Pharmacy
Lin Tan, Zhuo-Ya Zheng, Lv Huang, Zhong Jin, Su-Lian Li, Gui-Sheng Wu, Huai-Rong Luo
Summary: This study found that Complanatoside A (CA) could extend the lifespan of Caenorhabditis elegans and improve their physiological functions. CA also reduced the accumulation of toxic proteins and delayed the onset of neurodegenerative disorders. The study suggested that CA is a potential antiaging agent worth further research.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Environmental Sciences
Chi-Wei Huang, Wan-Ru Liao, Chun Ming How, Pei-Ling Yen, Chia-Cheng Wei
Summary: The study found that ZEN significantly decreased locomotive behaviors in C. elegans. Lifespan and aging markers were also adversely affected by ZEN, which increased ROS levels and downregulated antioxidant genes. Long-term exposure to ZEN induced aging-related decline in C. elegans, associated with oxidative stress and inhibition of antioxidant defense.
ENVIRONMENTAL POLLUTION
(2021)
Article
Food Science & Technology
Jiaqian Hong, Yiming Song, Jiayan Xie, Jianhua Xie, Yi Chen, Ping Li, Danyang Liu, Xiaobo Hu, Qiang Yu
Summary: This study used Caenorhabditis elegans as a model organism to investigate the toxic effects and mechanisms of acrolein (ACR) exposure. The results showed that ACR exposure shortened the lifespan of C. elegans, reduced reproductive capacity and locomotive behavior, and increased oxidative stress levels. ACR also affected the expression of antioxidant-related genes. The findings suggest that ACR exposure induces aging and oxidative stress in C. elegans, activating the DAF-16/FOXO pathway.
Article
Environmental Sciences
Pei -Ling Yen, Cai-Ru Yang, Mei-Lun Huang, Ting -An Lin, Vivian Hsiu-Chuan Liao
Summary: This study aims to evaluate the effects of chronic DEHP exposure on innate immunosenescence in C. elegans. The length of the exposure period significantly impacts DEHP-induced age-related declines, which is linked to immunosenescence and oxidative stress. DEHP exposure increases the expression of riok-1, a human RIO kinase homolog, which is associated with DEHP-induced HLH-30/TFEB translocation.
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
(2023)
Article
Medicine, Research & Experimental
Xingzhuo Song, Yu Du, Cen Liu, Wei Wang, Jing Han, Xinlou Chai, Yonggang Liu
Summary: Oxidative stress disrupts redox state homeostasis and induces apoptosis. Prolonged oxidative stress can impair cell, tissue, and organ function, leading to the development of diseases. H-2 synthesized from N-Alkylamides (NAAs) of Anacyclus pyrethrum (L.) DC was investigated for its antioxidant activity and molecular mechanisms using Caenorhabditis elegans (C. elegans) and B16-F10 mouse melanoma cell models. In vivo studies on C57BL/6 mice showed the anti-vitiligo activity of H-2. The results demonstrated that H-2 increased the survival time of nematodes under oxidative stress, promoted the nuclear localization of DAF-16, and enhanced the expression of Superoxide Dismutase 3 (SOD-3) in nematodes, thus activating the antioxidant enzyme system. H-2 also reversed oxidative stress damage in the B16-F10 cell model and increased the number of melanocytes in vitiligo model mice, suggesting its potential in vitiligo treatment.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Cell Biology
Benson Otarigho, Alejandro Aballay
Summary: Evidence suggests that the PITX/UNC-30 transcription factor in Caenorhabditis elegans regulates the tradeoff between immunity and longevity through a signaling pathway involving GATA/ELT-2, p38 MAPK/PMK-1, MXD/MDL-1, and PQM-1. This regulatory function of PITX/UNC-30 requires the sensory neuron ASG and a signaling pathway controlled by NPR-1, a G protein-coupled receptor related to mammalian neuropeptide Y receptors, revealing a suppressive role of GABAergic signaling in the neural control of energy allocation between immunity and longevity.
Article
Biochemistry & Molecular Biology
Zong-Ping Zhang, Xue Bai, Wen-Bo Cui, Xiao-Han Chen, Xu Liu, De-Juan Zhi, Zhan-Xin Zhang, Dong-Qing Fei, Dong-Sheng Wang
Summary: This study found that Caesalmin C can delay the progression of AD in the transgenic C. elegans model by inhibiting A beta deposition, upregulating the expression of genes associated with oxidative stress, inhibiting acetylcholinesterase activity, and upregulating proteasome activity.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)