Review
Biochemistry & Molecular Biology
Giandomenico Bisaccia, Fabrizio Ricci, Sabina Gallina, Angela Di Baldassarre, Barbara Ghinassi
Summary: The myocardium burns a significant amount of ATP within the mitochondria, crucial for its functions. Mitochondrial dysfunction is linked to a wide range of heart diseases and can contribute to the development of heart failure. Targeting mitochondrial function may be a potential treatment strategy for heart failure.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Pharmacology & Pharmacy
Guang-Qiong Zhang, Sheng-Quan Wang, Yan Chen, Ling-Yun Fu, Yi-Ni Xu, Ling Li, Ling Tao, Xiang-Chun Shen
Summary: Mitochondria are crucial organelles for cellular energy supply, and miRNAs play a key role in mediating cardiac diseases by regulating mitochondrial function-related genes. Understanding the crosstalk between miRNAs and mitochondria is important for the prevention and treatment of cardiac diseases.
FRONTIERS IN PHARMACOLOGY
(2021)
Review
Cell Biology
Alvaro A. Elorza, Juan Pablo Soffia
Summary: Cardiovascular diseases are common in elderly people. Research has shown that mitochondrial dysfunction, caused by the generation of reactive oxygen species, is the origin of aging-associated cardiovascular diseases. Increasing mitochondrial function by decreasing mtDNA heteroplasmy is crucial for preventing and delaying the development of these diseases.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Critical Care Medicine
Ran-Ran Zhang, Jing-Long Zhang, Qiao Li, Shu-Miao Zhang, Xiao-Ming Gu, Wen Niu, Jing-Jun Zhou, Lyu-Chen Zhou
Summary: Mitochondrial damage is a significant cause of heart dysfunction after severe burn injury, and the role of a cysteine protease called μ-calpain in this process has been investigated. Rats subjected to severe burn injury showed weakened heart performance and diminished mitochondrial function, along with increased levels of calpain in mitochondria. Treatment with the calpain inhibitor MDL28170 attenuated these responses to severe burn injury.
Review
Cell Biology
Teresa Campbell, Jesse Slone, Taosheng Huang
Summary: Mitochondria, responsible for generating energy in the form of ATP, have their own genetic material called mtDNA, along with nuclear genome, that determines their structure and function. Pathogenic variants in mtDNA or nuclear genome can cause mitochondrial disease, especially affecting high energy-demanding tissues like the heart. Mitochondrial cardiomyopathy, a result of genetic defects in either nDNA or mtDNA, manifests as hypertrophic or dilated cardiomyopathy and cardiac conduction defects. The complex pathophysiology of mitochondrial cardiomyopathy involves various abnormal processes such as deficient oxidative phosphorylation, ATP depletion, activation of alternative metabolic pathways, accumulation of reactive oxygen species, dysfunctional mitochondrial dynamics, abnormal calcium homeostasis, and mitochondrial iron overload.
Review
Cardiac & Cardiovascular Systems
Juntao Yang, Tingting Lv, Jiedong Zhou, Hui Lin, Bingjie Zhao, Haifei Lou, Hanxuan Liu, Tao Zhang, Hangyuan Guo, Jufang Chi
Summary: The study found that Ivabradine can reduce heart rate and ventricular volume, improving cardiac function in patients with DCM. However, it did not significantly affect the prognosis of patients.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2023)
Review
Cardiac & Cardiovascular Systems
Brian Schwartz, Petro Gjini, Deepa M. Gopal, Jessica L. Fetterman
Summary: Mitochondrial abnormalities and dysfunction play a significant role in the development of cardiomyopathies and heart failure. Recent studies have shown that heart failure with preserved ejection fraction may have distinct metabolic characteristics compared to heart failure with reduced ejection fraction. The mitochondrial ecosystem, consisting of intricate metabolic pathways and dynamic changes in mitochondrial networks and subcellular locations, is in delicate balance and disruptions in one component can have widespread effects on cellular pathways. Understanding the mitochondrial ecosystem in heart failure is crucial for developing therapeutics to improve outcomes.
JACC-BASIC TO TRANSLATIONAL SCIENCE
(2022)
Review
Pharmacology & Pharmacy
Chennan Wu, Zhen Zhang, Weidong Zhang, Xia Liu
Summary: Cardiovascular diseases, including heart failure, are leading causes of death globally. Despite advancements in therapies, life expectancy for heart failure remains poor. Targeting mitochondrial dysfunction, which is closely related to heart failure, may be an effective approach for treatment.
PHARMACOLOGICAL RESEARCH
(2022)
Review
Cardiac & Cardiovascular Systems
Christine M. Loescher, Anastasia J. Hobbach, Wolfgang A. Linke
Summary: This review provides an overview of the changes in cardiac titin properties at a molecular level, including the role isoform diversity and post-translational modifications play in regulating myocardial function, and discusses the importance of this regulation imbalance in heart disease.
CARDIOVASCULAR RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Carmine Rocca, Ernestina Marianna De Francesco, Teresa Pasqua, Maria Concetta Granieri, Anna De Bartolo, Maria Eugenia Gallo Cantafio, Maria Grazia Muoio, Massimo Gentile, Antonino Neri, Tommaso Angelone, Giuseppe Viglietto, Nicola Amodio
Summary: Mitochondria play a crucial role in maintaining myocardial tissue homeostasis and their impairments can lead to cardiovascular diseases. Anti-cancer drugs can induce mitochondrial toxicity, resulting in cell death.
Review
Oncology
Liyang Li, Ruixue Qi, Linlin Zhang, Yuexin Yu, Jiayun Hou, Yutong Gu, Dongli Song, Xiangdong Wang
Summary: Mitochondrial dysfunction plays a crucial role in cellular homeostasis and disease development, regulated by mitochondria-associated factors. The exploration of mitochondrial quality control system as potential diagnostic biomarkers and therapeutic targets for diseases could offer new insights.
CLINICAL AND TRANSLATIONAL MEDICINE
(2021)
Article
Cell Biology
Nasab Ghazal, Jessica N. Peoples, Tahmina A. Mohiuddin, Jennifer Q. Kwong
Summary: Contrary to previous beliefs, the adult heart shows remarkable resilience to acute insults to mtDNA regulation, maintaining mitochondrial function and cardiac function even with decreased TFAM protein levels. This resilience is only compromised with long-term TFAM inactivation, leading to mitochondrial dysfunction and cardiomyopathy.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2021)
Article
Cell Biology
Qixin Chen, Liu-Yi Liu, Zhiqi Tian, Zhou Fang, Kang-Nan Wang, Xintian Shao, Chengying Zhang, Weiwei Zou, Fiona Rowan, Kangqiang Qiu, Baohua Ji, Jun-Lin Guan, Dechang Li, Zong-Wan Mao, Jiajie Diao
Summary: In this study, a dual-color fluorescent probe called mtGLP was developed to monitor the dynamics of mitochondrial membrane and mtDNA simultaneously. Through experiments and simulations, it was discovered that nucleoid condensates utilize peripheral fission to maintain mitochondrial homeostasis.
Review
Biology
Giampaolo Morciano, Veronica Angela Maria Vitto, Esmaa Bouhamida, Carlotta Giorgi, Paolo Pinton
Summary: The heart is crucial for the circulation of blood and oxygen in the body, and its function relies on a delicate balance of energy consumption and generation. Mitochondrial dysfunctions have been identified as key factors in the development of various heart diseases, particularly heart failure.
Article
Cardiac & Cardiovascular Systems
Yu-Han Chen, Albert P. Ta, Yumay Chen, Hsiao-Chen Lee, Wenjun Fan, Phang-Lang Chen, Maria C. Jordan, Kenneth P. Roos, Grant R. MacGregor, Qin Yang, Robert A. Edwards, Junfeng Li, Ping H. Wang
Summary: The study aimed to investigate the effect of mitochondrial AKT signaling on cardiac structure and function. The results showed that disrupted mitochondrial AKT signaling led to cardiomyopathy with cardiac fibrosis, left ventricular hypertrophy, and dysfunction. On the other hand, activation of mitochondrial AKT1 protected against diabetic cardiomyopathy and improved overall metabolism. These findings highlight the importance of mitochondrial AKT signaling in maintaining cardiac health.
CARDIOVASCULAR DIABETOLOGY
(2023)
Review
Management
Elton H. Lobo, Mohamed Abdelrazek, Finn Kensing, Lene J. Rasmussen, Patricia M. Livingston, John Grundy, Sheikh Mohammed Shariful Islam, Anne Frolich
Summary: This rapid review examined technology-based interventions for stroke caregivers in the literature and found that most interventions showed positive results in terms of impact, acceptance, effectiveness, and satisfaction.
JOURNAL OF NURSING MANAGEMENT
(2022)
Article
Genetics & Heredity
Oyvind P. Haugena, Cuong M. Khuu, Hanne M. Weidemann, Tor Paaske Utheim, Linda Hildegard Bergersen
Summary: In pancreatic ductal adenocarcinoma (PDAC), the lactate receptor HCAR1 is highly expressed and regulated by miRNA miR-431-5p. Overexpression of miR-431-5p inhibits cell proliferation, induces cell cycle progression changes and apoptosis in PDAC cells. Transcriptomic analysis reveals that numerous differentially expressed genes (DEGs), especially ATP6V0E1, are involved in cancer-related processes and signaling pathways. Knockdown of ATP6V0E1, instead of HCAR1, mimics the effects of miR-431-5p overexpression on cell viability in PDAC cells.
Article
Multidisciplinary Sciences
Elton H. Lobo, Tara Johnson, Anne Frolich, Finn Kensing, Lene J. Rasmussen, Sarah M. Hosking, Amy T. Page, Patricia M. Livingston, Sheikh Mohammed Shariful Islam, John Grundy, Mohamed Abdelrazek
Summary: The study found a significant increase in the use of social media by caregivers of stroke patients. The most popular social media communities for stroke care information were charitable and governmental organizations, with the highest user interaction for topics such as stroke prevention, signs and symptoms, and caregiver self-care delivered through video-based resources.
Article
Cell Biology
Peng Song, Shaojun Liu, Dekang Liu, Guido Keijzers, Daniela Bakula, Shunlei Duan, Niels de Wind, Zilu Ye, Sergey Y. Vakhrushev, Morten Scheibye-Knudsen, Lene Juel Rasmussen
Summary: DNA mismatch repair (MMR) is an important DNA repair pathway that, when defective, is linked to carcinogenesis and drug resistance. This study demonstrates that depletion of CNOT6, which is overexpressed in cancer cells, sensitizes cells to DNA damage and enhances apoptosis. Depletion of CNOT6 also upregulates MMR and decreases mutation frequency, possibly through stabilizing mRNA transcripts from MMR genes and increasing MMR protein expression.
Article
Oncology
Christine Hjorth Andreassen, Mette Lorenzen, John E. Nielsen, Sam Kafai Yahyavi, Birgitte Gronkaer Toft, Lars R. Ingerslev, Christoffer Clemmensen, Lene Juel Rasmussen, Carsten Bokemeyer, Anders Juul, Anne Jorgensen, Martin Blomberg Jensen
Summary: This study shows that inhibition of the RANKL signalling system can suppress tumor growth in human TGCTs, but different effects were observed in different cell types. Serum RANKL has no prognostic value in TGCT patients.
BRITISH JOURNAL OF CANCER
(2022)
Article
Cell Biology
Claus Desler, Jon Ambaek Durhuus, Thomas Lau-Lindestrand Hansen, Sharath Anugula, Nadia Thaulov Zelander, Sisse Boggild, Lene Juel Rasmussen
Summary: The correlation between mitochondrial function and oncogenesis is complex and not fully understood. This study demonstrates that inhibition of mitochondrial-linked pyrimidine synthesis in cancer cells results in a more aggressive tumor phenotype, without affecting DNA repair ability.
Article
Oncology
Mrinal K. Das, Oyvind P. Haugen, Trine B. Haugen
Summary: Testicular germ cell tumour (TGCT) is the most common cancer type among young adults in many parts of the world. MicroRNAs (miRNAs), a class of non-coding RNAs, play important roles in TGCT pathogenesis by regulating gene expression at the post-transcriptional level. They can act as either oncogenes or tumour suppressors by influencing cellular processes such as proliferation, differentiation, and apoptosis. The involvement of miRNAs in TGCT development has been supported by differential expression studies and functional studies that explore individual miRNA targets and downstream pathways. This review summarises the diverse roles and targets of miRNAs in TGCT pathogenesis.
Article
Biochemistry & Molecular Biology
Nicolas A. Pinto, Martin C. Abba, Lorena Laporte, Juan M. Perez M. Saez, Ada G. G. Blidner, Nicolas I. Torres, Rosa M. M. Morales, Sabrina G. G. Gatto, Camila A. A. Bach, Florencia Veigas, Hernan J. Garcia Rivello, Peng Song, Jane H. H. Frederiksen, Lene Juel Rasmussen, Francoise Poirier, Diego O. O. Croci, Victoria Sundblad, Gabriel A. A. Rabinovich, Juan P. P. Cerliani
Summary: Non-melanoma skin cancer (NMSC) has increased due to chronic exposure to sunlight, climatic changes, and immunosuppression. Gal-7, a protein expressed in skin tissue, plays a critical role in NMSC development. Overexpression of Gal-7 leads to an increase in the number of papillomas in transgenic mice.
CELL DEATH AND DIFFERENTIATION
(2023)
Article
Biochemistry & Molecular Biology
Sima Zolfaghari, Ole Jorgen Kaasboll, Vivi T. Monsen, Bojana Sredic, Else Marie V. Hagelin, Havard Attramadal
Summary: Cellular Communication Network (CCN) proteins play important roles in cellular responses associated with organ development and tissue homeostasis. CCN5, a divergent member of the CCN family, releases the TSP1 homology domain as its bioactive signaling entity, and inhibits key signaling pathways stimulated by CCN2. Moreover, the CCN5 TSP1 domain also inhibits cell migration and scratch wound closure induced by CCN1/2.
JOURNAL OF BIOLOGICAL CHEMISTRY
(2023)
Article
Multidisciplinary Sciences
Elton H. J. Lobo, Anne Frolich, Mohamed M. Abdelrazek, Lene J. Rasmussen, John Grundy, Patricia M. Livingston, Sheikh Mohammed Shariful Islam, Finn Kensing
Summary: This study identifies the needs of stroke caregivers, including information, involvement in decision-making, self-care, and support. It highlights the importance of a caregiver-centered approach in stroke recovery to reduce uncertainty and burden of care.
Article
Geriatrics & Gerontology
Taoyu Mei, Yuan Li, Anna Orduna Dolado, Zhiquan Li, Robin Andersson, Laura Berliocchi, Lene Juel Rasmussen
Summary: The growing prevalence of Alzheimer's disease (AD) is a global health challenge without effective treatments. Defective mitochondrial function and mitophagy have been suggested as etiological factors in AD. This study integrated transcriptomic data from AD and healthy patients to identify mitophagy-related genes and validate their expression changes in AD-relevant human in vitro models.
FRONTIERS IN AGING NEUROSCIENCE
(2023)
Review
Cell Biology
Vivi Talstad Monsen, Havard Attramadal
Summary: CCN proteins are important in development, tissue injury repair, and cancer metastasis. Their molecular mechanisms of action are still poorly understood, but recent research has shown that they are signaling proteins that can be controlled to release bioactive peptides. The crystal structure of CCN3 domains and predictions from the AlphaFold tool provide new insights into CCN functions. Understanding the structure-function relationship of CCN proteins is crucial for developing therapeutic strategies.
JOURNAL OF CELL COMMUNICATION AND SIGNALING
(2023)
Article
Public, Environmental & Occupational Health
Elton H. Lobo, Mohamed Abdelrazek, Anne Frolich, Lene J. Rasmussen, Patricia M. Livingston, Sheikh Mohammed Shariful Islam, Finn Kensing, John Grundy
Summary: This study aims to identify the user experience issues of stroke caregiving apps by analyzing user reviews, in order to guide future app development. The findings highlight critical issues that decrease user satisfaction and increase frustration, emphasizing the importance of understanding user needs during the development process.
FRONTIERS IN PUBLIC HEALTH
(2023)
Article
Multidisciplinary Sciences
Sharath Anugula, Zhiquan Li, Yuan Li, Alexander Hendriksen, Peter Bjarn Christensen, Lin Wang, Jonathan M. Monk, Niels de Wind, Vilhelm A. Bohr, Claus Desler, Robert K. Naviaux, Lene Juel Rasmussen
Summary: Rev1 deficiency leads to metabolic dysregulation and mitochondrial anomalies, and these phenotypes can be improved by NAD+ supplementation. Autophagy decreases in Rev1-/- MEFs and can be restored by supplementing the NAD+ precursor NR. Abnormal mitochondrial morphology in Rev1-/- MEFs can be partially reversed by NR supplementation, and it also protects the mitochondrial cristae from rotenone-induced degeneration. However, NR supplementation cannot rescue the sensitivity to oxidative stress caused by rev-1 deficiency in nematodes.
Review
Cell Biology
Yuan Li, Laura Berliocchi, Zhiquan Li, Lene Juel Rasmussen
Summary: Current research on human aging has been guided by the hallmarks of aging proposed in 2013. Most studies have focused on individual hallmarks, but recent research has explored the complex interactions between multiple hallmarks and their effects over time. Understanding these interconnections will greatly benefit aging research and the development of effective interventions for promoting healthy aging.