Article
Cell Biology
Luca Giordano, Alyssa D. Gregory, Mireia Perez Verdaguer, Sarah A. Ware, Hayley Harvey, Evan DeVallance, Tomasz Brzoska, Prithu Sundd, Yingze Zhang, Frank C. Sciurba, Steven D. Shapiro, Brett A. Kaufman
Summary: This study measured the levels of cf-mtDNA and cf-nDNA in the plasma of COPD patients and the serum of mice with CS-induced emphysema and found increased levels of cf-mtDNA in both. In cell culture, exposure to CSE resulted in decreased mitochondrial membrane potential, increased oxidative stress, dysregulated mitochondrial dynamics, and triggered mtDNA release in extracellular vesicles. These findings suggest that cf-mtDNA could serve as a marker of mitochondrial stress in response to CS exposure and COPD pathology.
Review
Cell Biology
Yongyu He, Wenqing Xie, Hengzhen Li, Hongfu Jin, Yi Zhang, Yusheng Li
Summary: Aging promotes degenerative pathologies in mammals, including sarcopenia. New findings suggest that age-related sarcopenia can be delayed by modulating mechanisms such as cellular senescence. Studies have shown that targeting cellular senescence is an effective strategy for alleviating sarcopenia. However, more research is needed to understand the mechanisms through which senescent cells contribute to sarcopenia progression.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Cornelius Engelmann, Frank Tacke
Summary: Cellular senescence plays a significant role in non-alcoholic fatty liver disease (NAFLD), but further research is needed to understand the specific mechanisms. Hepatocyte senescence may contribute to fat accumulation, fibrosis, and inflammation, while senescence in non-parenchymal liver cells could potentially reduce fibrosis. A comprehensive understanding of the interaction between NAFLD and cellular senescence is crucial for identifying novel therapeutic targets.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Helene Martini, Joao F. Passos
Summary: The article discusses how the accumulation of senescent cells in multiple tissues leads to tissue dysfunction and age-related diseases, and emphasizes the important role and mechanisms of mitochondria in senescence. It also proposes the establishment of a detailed road map of mitochondrial biology to guide future research on treatments.
Review
Medicine, General & Internal
Rongjun Wan, Prakhyath Srikaram, Vineeta Guntupalli, Chengping Hu, Qiong Chen, Peisong Gao
Summary: Asthma is a chronic respiratory disease affecting approximately 10% of the global population. The accumulation of senescent cells has been identified as a trigger for the pathophysiology of asthma. This review focuses on the relationship between cellular senescence and asthma, including triggers such as telomere shortening, DNA damage, oncogene activation, oxidative-related senescence, and senescence-associated secretory phenotype (SASP). The connection between cellular senescence and asthma phenotypes, including airway inflammation and remodeling, is also discussed. Promising approaches targeting cellular senescence, such as senolytics and senomorphics, have emerged as potential strategies for asthma treatment.
Article
Cell Biology
Irene Lopez-Antona, Constanza Contreras-Jurado, Laura Luque-Martin, Antonio Carpintero-Leyva, Paula Gonzalez-Mendez, Ignacio Palmero
Summary: Cellular senescence has a significant impact on the regulation of the myofibroblastic phenotype in primary fibroblasts. The loss of myofibroblastic markers and functional features upon senescence implementation can be transmitted in a paracrine manner, most likely through soluble secreted factors. The Notch/TGF-beta axis is found to be the main pathway mediating the changes in the myofibroblast phenotype.
Review
Oncology
Andreas Domen, Christophe Deben, Jasper Verswyvel, Tal Flieswasser, Hans Prenen, Marc Peeters, Filip Lardon, An Wouters
Summary: Cellular senescence is a mechanism in which cells enter a state of stable cell-cycle arrest with secretory features in response to cellular stress. It has been historically seen as a protective mechanism against cancer by eliminating damaged cells. However, the accumulation of senescent cells can have long-term detrimental effects and contribute to age-related diseases, including cancer. The role of cellular senescence in cancer is ambiguous and controversial, and its detection and study in cancer patients present challenges. This review highlights the methods and challenges of detecting cellular senescence in cancer patients, and discusses its prognostic implications.
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Donghui Zhang, Yanmei Zhu, Yanmin Ju, Hongyong Zhang, Xiaopeng Zou, Shangrong She, Danping Zhu, Yiting Guan
Summary: Dramatic changes in chromatin structure occur during cellular senescence, affecting genome accessibility and transcription. This study investigates the redistribution of accessible chromatin regions during senescence and identifies the transcription factor TEAD4 as a key regulator of chromatin state and SASP gene transcription.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2023)
Editorial Material
Biochemistry & Molecular Biology
Darren J. Baker, Masashi Narita, Pura Munoz-Canoves
Summary: The contribution of cellular senescence in various biological processes has been overlooked but is now gaining attention. This Editorial provides an overview of the review and original work articles in The FEBS Journal's Special Issue on Senescence in Ageing and Disease. Senescent cells have both positive and negative effects on tissue injury, aging, and pathology. The identification of senescent cells has improved, especially in slow-proliferating or terminally differentiated tissues. The communication between senescent cells and other tissue residents, as well as the role of the senescence-associated secretory phenotype (SASP), are important topics in this Special Issue.
Review
Biology
Sijia Chen, Dian Zhou, Ousheng Liu, Huan Chen, Yuehong Wang, Yueying Zhou
Summary: Oral health plays a crucial role in overall health, and tooth loss is closely associated with aging and periodontitis. Targeting cellular senescence may offer potential therapeutic strategies for age-related conditions, including tooth loss. This review explores the role of cellular senescence in oral health and discusses potential treatment options for excessive alveolar bone loss in periodontitis.
Review
Cell Biology
Vivekananda Budamagunta, Thomas C. Foster, Daohong Zhou
Summary: Immunosenescence is a complex phenomenon that leads to age-related immune dysfunction, resulting in various pathologies such as decreased ability to clear senescent and cancerous cells, increased autoimmune response, reduced ability to combat pathogens, and diminished response to vaccination. Cellular senescence and immunosenescence have not been extensively explored in terms of their relationship, yet in the context of the ongoing pandemic, immunosenescence has become a topic of great importance.
Review
Biochemistry & Molecular Biology
Georgia Bateman, Hong Guo-Parke, Aoife M. Rodgers, Dermot Linden, Melanie Bailey, Sinead Weldon, Joseph C. Kidney, Clifford C. Taggart
Summary: Cellular senescence is a state of permanent cell cycle arrest triggered by various stressors, and its accumulation has been observed in many age-related diseases. In chronic obstructive pulmonary disease (COPD), airway epithelium exhibits hallmark features of senescence, leading to cell cycle arrest and secretion of inflammatory mediators that contribute to chronic inflammation. Additionally, cellular senescence in COPD airway epithelium is associated with telomere dysfunction, DNA damage, and oxidative stress. Understanding the mechanisms and impact of cellular senescence in COPD may provide potential therapeutic targets for this disease.
Review
Cell Biology
Dilara Demirci, Bengisu Dayanc, Fatma Aybuke Mazi, Serif Senturk
Summary: Cellular senescence is a state of stable cell cycle arrest triggered by various insults, with potential adverse implications such as inflammation, cancer stemness, senescence reversal, therapy resistance, and disease recurrence, which can be mitigated by eliminating senescent cells or inhibiting their SASP production to enhance cancer therapy efficacy.
Review
Biochemistry & Molecular Biology
Priyanka Banerjee, Niyanshi Gaddam, Tej K. Pandita, Sanjukta Chakraborty
Summary: Cellular senescence, driven by various mechanisms and senescence-associated secretory phenotype (SASP), is an important area of research in age-related diseases. The impact of senescence and SASP on different cell types, the immune system, and the vascular system has been widely discussed, but the impact on lymphatic biology and pathological lymphangiogenesis remains underexplored. In this review, the role of senescence on lymphatic pathobiology, its impact on cancer, and potential therapeutic interventions are discussed.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Michela Cortesi, Michele Zanoni, Francesca Pirini, Maria Maddalena Tumedei, Sara Ravaioli, Ilario Giovanni Rapposelli, Giovanni Luca Frassineti, Sara Bravaccini
Summary: Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis due to immune suppression and the tumor microenvironment. This review explores the interplay between senescent and non-senescent cell types and their impact on PDAC progression. The non-tumoral cells in the tumor microenvironment influence key aspects of tumor growth, metabolism, cell death, and treatment resistance. Understanding these interactions is crucial for PDAC treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Dhirendra Pratap Singh, Rizwana Begum, Gagandeep Kaur, Prathyusha Bagam, Devaiah Kambiranda, Rakesh Singh, Sanjay Batra
Summary: Electronic cigarettes (e-cigs) are popular battery-operated heating devices that are marketed as a safer alternative to traditional cigarettes. However, recent reports of lung injuries associated with e-cig use have sparked a debate on the potential harms of vaping. Researchers are increasing their efforts to understand the effects of vaping on human health, including the inflammatory response and pulmonary health issues caused by e-cigs.
CELL BIOLOGY AND TOXICOLOGY
(2021)
Article
Physiology
Gagandeep Kaur, Shaiesh Yogeswaran, Thivanka Muthumalage, Irfan Rahman
Summary: The study revealed that smokers have higher serum levels of ACE2 and ACE2 enzyme activity in COVID-19 infection, while the levels of Ang1-7 in the serum of COVID-19 patients are also significantly elevated. Smoking also leads to an increase in inflammatory markers and COVID-19 associated proteins in the serum of COVID-19 patients.
FRONTIERS IN PHYSIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Krishna Prahlad Maremanda, Isaac Kirubakaran Sundar, Irfan Rahman
Summary: The study found that short OPA1 isoforms are increased in COPD patients, and acute cigarette smoke exposure leads to conversion of long to short OPA1 isoforms in various cell lines. Mitochondrial stress-related protein SLP2 was significantly increased in all cells following cigarette smoke exposure. Treatment with certain compounds like BGP-15 and leflunomide could preserve the long OPA1 isoform in cells exposed to cigarette smoke. These findings suggest that long OPA1 isoform, along with SLP2 and prohibitins, may play a crucial role in cigarette smoke-induced lung damage in COPD.
Letter
Allergy
Isaac Kirubakaran Sundar, Ashokkumar Srinivasan
CLINICAL AND TRANSLATIONAL ALLERGY
(2021)
Article
Medicine, Research & Experimental
Qixin Wang, Isaac K. Sundar, Joseph H. Lucas, Thivanka Muthumalage, Irfan Rahman
Summary: This study investigated the role of REV-ERBα in circadian dysfunction and EMT alteration induced by cigarette smoke. The results showed that REV-ERBα agonist could alleviate CS-induced inflammation and abnormal EMT in the lungs, suggesting activation of REV-ERBα as a potential novel therapeutic approach for smoking-induced chronic inflammatory lung diseases.
Article
Biochemistry & Molecular Biology
Qixin Wang, Xiangming Ji, Irfan Rahman
Summary: The study showed that e-cig vaping and cigarette smoking have distinct effects on systemic metabolites. E-cig vaping dysregulates TCA cycle-related metabolites, while cigarette smoking alters sphingolipid metabolites. Both e-cig and cigarette smoke increase nicotinic metabolites.
Article
Biochemistry & Molecular Biology
Gagandeep Kaur, Krishna Prahlad Maremanda, Michael Campos, Hitendra S. Chand, Feng Li, Nikhil Hirani, M. A. Haseeb, Dongmei Li, Irfan Rahman
Summary: The study investigated the miRNA profiles of lung-tissue-derived exosomes in COPD and IPF patients, revealing miRNA downregulation in exosomes derived from the lung tissue of COPD patients, while a large number of differentially expressed miRNAs were found in exosomes derived from the lung tissue of IPF patients.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Editorial Material
Environmental Sciences
Dimitrios Michelogiannakis, Irfan Rahman
INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
(2022)
Article
Environmental Sciences
Shaiesh Yogeswaran, Irfan Rahman
Summary: There are differences in the generation of reactive oxygen species (ROS) between tobacco-free nicotine (TFN) e-cigarettes and e-cigarettes using tobacco-derived nicotine, with TFN tobacco and fruit flavors showing higher levels of toxicity.
Article
Environmental Sciences
Thomas Lamb, Thivanka Muthumalage, Jiries Meehan-Atrash, Irfan Rahman
Summary: This study found that flavoring chemicals in electronic cigarettes can cause lung inflammation, and the effects of fruit and tobacco flavors on lung inflammation in mice are still unknown. The results showed that exposure to cherry-flavored e-liquids in female mice and tobacco-flavored e-liquids in male mice increased lung inflammation.
Article
Environmental Sciences
Sadiya Bi Shaikh, Wai Cheung Tung, Cortney Pang, Joseph Lucas, Dongmei Li, Irfan Rahman
Summary: Oral nicotine pouches (ONPs) are a modern form of smokeless tobacco products. Flavored ONPs may cause adverse effects on oral and respiratory epithelial cells, leading to inflammation and toxicological responses.
Article
Pathology
Shikha Sharma, Qixin Wang, Thivanka Muthumalage, Irfan Rahman
Summary: Mitochondrial quality control is maintained by Miro1, a calcium-binding GTPase, during mitophagy. The presence of Miro1 appears to regulate lung inflammation induced by cigarette smoke exposure through its interaction with mitophagy machinery. The findings suggest that Miro1 may play a critical role in mitigating lung inflammatory responses associated with mitochondrial dysfunction caused by cigarette smoke.
Article
Cell Biology
Prathyusha Bagam, Gagandeep Kaur, Dhirendra Pratap Singh, Sanjay Batra
Summary: Cigarette smoking is the primary cause of chronic obstructive pulmonary disease. Oxidative stress induced by cigarette smoke leads to abnormal autophagy, resulting in acute lung injury. The study highlights the crucial role of FOXO1 and FOXO3a in regulating autophagy in response to cigarette smoke exposure.
CELL BIOLOGY AND TOXICOLOGY
(2021)