Article
Environmental Sciences
Jung-Min Park, Haerin Jeong, Yoon-Seok Seo, Van Quan Do, Seong-Jin Choi, Kyuhong Lee, Kyung-Chul Choi, Won Jun Choi, Moo-Yeol Lee
Summary: The presence of bicarbonate in the experimental conditions influences the superoxide generation induced by cigarette smoke, with peroxidase treatment reducing more than half of the superoxide production. This suggests that peroxides and peroxy acids are the main contributors to superoxide production in this process.
Article
Multidisciplinary Sciences
Ivan Menendez-Montes, Salim Abdisalaam, Feng Xiao, Nicholas T. Lam, Shibani Mukherjee, Luke I. Szweda, Aroumougame Asaithamby, Hesham A. Sadek
Summary: Mitochondrial utilization of fatty acids induces a significant increase in ROS detection at the chromatin level, indicating that mitochondrial metabolic perturbations directly alter the nuclear redox status, with chromatin being particularly sensitive to the prooxidant effect of FA utilization by the mitochondria.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Environmental Sciences
En-Ming Chang, Chia-Chia Chao, Mei-Ting Wang, Chia-Lang Hsu, Po-Chun Chen
Summary: PM2.5 exposure causes mitochondrial fragmentation and induces pulmonary fibrosis in type II alveolar cells, leading to collagen accumulation in lung tissue.
ENVIRONMENTAL TOXICOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Yue Zhang, Wenhui Huang, Zemao Zheng, Wei Wang, Yafei Yuan, Qiaohui Hong, Jiajia Lin, Xu Li, Ying Meng
Summary: Cigarette smoke induces senescence of AT2 cells via a SIRT1/autophagy dependent pathway, involving mitochondrial reactive oxygen species and DNA damage. Activating SIRT1 can reduce senescence by promoting autophagy.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Review
Biochemistry & Molecular Biology
Yoon-Seok Seo, Jung-Min Park, Jae-Hyeong Kim, Moo-Yeol Lee
Summary: Smoking is a significant risk factor for various diseases due to the production of excessive reactive oxygen species (ROS). This review focuses on how cigarette smoke promotes the formation of ROS and provides key mechanisms involved.
Review
Biochemistry & Molecular Biology
John O. Onukwufor, Robert T. Dirksen, Andrew P. Wojtovich
Summary: Alzheimer's disease is a neurodegenerative disease characterized by neuronal dysfunction and memory and cognitive decline. Iron dysregulation and iron-dependent cell death are associated with AD. Targeting ferroptosis, a specific form of cell death, may be a potential therapeutic intervention for AD.
Article
Pharmacology & Pharmacy
Jing Chang, Jiahui Wang, Beibei Luo, Weihao Li, Ziyue Xiong, Chaoqi Du, Xue Wang, Yuejiao Wang, Jingya Tian, Shuxin Li, Yue Fang, Longjie Li, Jing Dong, Ke Tan, Yumei Fan, Pengxiu Cao
Summary: This study found that VE significantly delayed the progression of BLM-induced PF and increased the survival rates of experimental mice. VE inhibited the pathological activation and fibrotic differentiation of lung fibroblasts, alleviated the inflammatory response, and protected against mitochondrial dysmorphology. Furthermore, VE suppressed apoptosis in BLM-PF lungs and pulmonary epithelial cells.
FRONTIERS IN PHARMACOLOGY
(2023)
Article
Pharmacology & Pharmacy
Shuxin Li, Hongmin Zhang, Jing Chang, Dongming Li, Pengxiu Cao
Summary: Pulmonary fibrosis is a chronic, progressive lung disease with limited treatment options. Recent research has shown that iron accumulation and mitochondrial damage play key roles in its development, highlighting a promising direction for finding effective therapeutics.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2021)
Review
Cell Biology
Ying Guo, Teng Guan, Kashfia Shafiq, Qiang Yu, Xin Jiao, Donghui Na, Meiyu Li, Guohui Zhang, Jiming Kong
Summary: Aging is a complex process involving functional decline in multiple organelles. The role of mitochondrial quality control (MQC) in aging is still poorly understood, although mitochondrial dysfunction is suggested to be a determining factor. Evidence suggests that reactive oxygen species (ROS) stimulate changes in mitochondrial dynamics and contribute to the accumulation of oxidized by-products through mitochondrial proteases and mitochondrial unfolded protein response (UPRmt). MQC mechanisms such as mitochondrial-derived vesicles (MDVs) and mitophagy play crucial roles in maintaining mitochondrial homeostasis and preventing cellular senescence and aging. However, imbalanced MQC interventions may accelerate abnormal energy metabolism and senescence. Appropriate interventions on MQC may delay the aging process and extend lifespan.
AGEING RESEARCH REVIEWS
(2023)
Article
Biochemistry & Molecular Biology
James H. Schofield, Zachary T. Schafer
Summary: The relationship between mitophagy and ROS production is complex and not fully understood. This review discusses mtROS generation and their detrimental effects on cellular viability, along with the cellular defense mechanisms against oxidative stress. Furthermore, the prominent mechanisms governing mitophagy induction that bear on oxidative stress are explored.
ANTIOXIDANTS & REDOX SIGNALING
(2021)
Article
Oncology
Gajalakshmi Ramanathan, Jane H. Chen, Nitya Mehrotra, Tiffany Trieu, Aaron Huang, Eduard Mas, Jessica Monterrosa E. Mena, Bishop Bliss, David A. Herman, Michael T. Kleinman, Angela G. Fleischman
Summary: Smoking is associated with clonal hematopoiesis of indeterminate potential (CHIP) which increases the risk of hematologic malignancy and cardiovascular disease. This study showed that smoking induces an inflammatory response in the bone marrow environment, promoting clonal expansion of existing gene mutations in hematopoietic stem cells.
FRONTIERS IN ONCOLOGY
(2023)
Article
Cardiac & Cardiovascular Systems
Sara Ranjbarvaziri, Kristina B. Kooiker, Mathew Ellenberger, Giovanni Fajardo, Mingming Zhao, Alison Schroer Vander Roest, Rahel A. Woldeyes, Tiffany T. Koyano, Robyn Fong, Ning Ma, Lei Tian, Gavin M. Traber, Frandics Chan, John Perrino, Sushma Reddy, Wah Chiu, Joseph C. Wu, Joseph Y. Woo, Kathleen M. Ruppel, James A. Spudich, Michael P. Snyder, Kevin Contrepois, Daniel Bernstein
Summary: The study found that metabolic signaling disruption and mitochondrial dysfunction are common pathogenic mechanisms in patients with HCM, highlighting potential new drug targets for mitigating the disease by improving metabolic function and reducing mitochondrial injury.
Article
Biochemistry & Molecular Biology
Jing Xiong, Yanqing Le, Yafei Rao, Lu Zhou, Yuhan Hu, Suliang Guo, Yongchang Sun
Summary: The RANKL/RANK pathway plays an important role in muscle atrophy induced by COPD-related lung diseases, suggesting that it may be a potential therapeutic target for COPD-related skeletal muscle dysfunction.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2021)
Review
Cell Biology
Jielin Deng, Yunqiu Jiang, Zhen Bouman Chen, June-Wha Rhee, Yingfeng Deng, Zhao V. Wang
Summary: Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are responsible for producing ATP, which is essential for the continuous electrical activity in the heart. Impaired supply-demand relationship and progressive mitochondrial dysfunction in arrhythmias result in reduced ATP production and increased reactive oxidative species generation. Pathological changes in gap junctions and inflammatory signaling disrupt ion homeostasis, membrane excitability, and cardiac structure, leading to impaired cardiac electrical homeostasis. This review focuses on the electrical and molecular mechanisms of cardiac arrhythmias, highlighting the role of mitochondrial dysfunction in ionic regulation and gap junction action. The article explores inherited and acquired mitochondrial dysfunction and its impact on different types of arrhythmias, as well as the involvement of mitochondria in bradyarrhythmia and tachyarrhythmia caused by factors like aging, gut microbiome, cardiac reperfusion injury, and electrical stimulation.
Article
Biochemistry & Molecular Biology
Mun-Ock Kim, Jae-Won Lee, Jae Kyoung Lee, Yu Na Song, Eun Sol Oh, Hyunju Ro, Dahye Yoon, Yun-Hwa Jeong, Ji-Yoon Park, Sung-Tae Hong, Hyung Won Ryu, Su Ui Lee, Dae Young Lee
Summary: Korean black ginseng extract inhibits airway inflammation and mucus secretion by decreasing the activation of TAK1, suggesting it could be a potential adjuvant in the treatment of airway inflammatory diseases caused by cigarette smoke.