Article
Biochemistry & Molecular Biology
Naris Thengchaisri, Lih Kuo, Travis W. Hein
Summary: In diabetes, the increased activity of the enzyme arginase competes with endothelial nitric oxide synthase (eNOS) for their common substrate L-arginine, leading to compromised vasodilation mediated by nitric oxide (NO). However, eNOS uncoupling in diabetes may result in the production of superoxide and compensatory hydrogen peroxide (H2O2) formation to restore NO deficiency. This study found that in early type 1 diabetes, the vasodilation response in coronary arterioles was partially impaired due to reduced availability of L-arginine as a result of upregulated arginase activity. Nevertheless, the increased production of H2O2 during eNOS uncoupling and PI3K activation seemed to compensate for the NO deficiency and mask the disturbance caused by arginase activation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Anna Janaszak-Jasiecka, Agata Ploska, Joanna M. M. Wieronska, Lawrence W. W. Dobrucki, Leszek Kalinowski
Summary: Nitric oxide (NO) is a crucial molecule released by endothelial cells that plays a significant role in cardiovascular homeostasis. Reduced availability of NO due to endothelial dysfunction is a common characteristic of cardiovascular disease. Risk factors such as diabetes, dyslipidemia, hypertension, aging, and smoking contribute to oxidative stress, which impairs the activity of endothelial nitric oxide synthase (eNOS) and leads to eNOS uncoupling. Uncoupled eNOS produces harmful free radicals instead of NO, exacerbating oxidative stress. This article explores the mechanisms of eNOS uncoupling and potential therapeutic approaches to prevent it.
CELLULAR & MOLECULAR BIOLOGY LETTERS
(2023)
Article
Biology
Yiying Wang, Qiannan Li, Zhiyang Zhang, Kai Peng, Dai-Min Zhang, Qianlu Yang, Anthony G. Passerini, Scott I. Simon, ChongXiu Sun
Summary: Inhibition of endothelium-specific mTOR complexes impairs endothelial-dependent vasodilation and reduces nitric oxide bioavailability. This is due to suppressed eNOS gene expression and increased reactive oxygen species production. Restoring KLF2 expression or suppressing Nox2 can reverse the impaired vasodilation in mice with inhibited mTOR complexes.
COMMUNICATIONS BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Vasiliy I. Vladimirov, Margarita P. Shchannikova, Alexey V. Baldin, Alexey S. Kazakov, Marina P. Shevelyova, Aliya A. Nazipova, Viktoriia E. Baksheeva, Ekaterina L. Nemashkalova, Anastasia S. Frolova, Natalia K. Tikhomirova, Pavel P. Philippov, Andrey A. Zamyatnin, Sergei E. Permyakov, Dmitry V. Zinchenko, Evgeni Yu. Zernii
Summary: The formation of the complex between Caveolin-1 and recoverin is regulated by redox state. The high affinity interaction of thiol-oxidized recoverin with Caveolin-1 may affect the translocation and desensitization of visual proteins.
Article
Oncology
Silvia Codenotti, Francesco Marampon, Luca Triggiani, Marco Lorenzo Bonu, Stefano Maria Magrini, Paola Ceccaroli, Michele Guescini, Stefano Gastaldello, Vincenzo Tombolini, Pietro Luigi Poliani, Michela Asperti, Maura Poli, Eugenio Monti, Alessandro Fanzani
Summary: The study investigated the role of Caveolin-1 (Cav-1) in radiation response in rhabdomyosarcoma (RMS), suggesting that Cav-1 may play a vital role in promoting radioresistance through mechanisms involving cell cycle regulation, apoptosis, oxidative stress and DNA repair pathways. The findings reveal that Cav-1, in conjunction with catalase, Src-kinase, and Akt pathways, may form a network of essential mechanisms that allow irradiated RMS cells to evade cell death induced by radiation.
Article
Cell Biology
Andreas Goutas, Zozo Outskouni, Ioanna Papathanasiou, Maria Satra, George Koliakos, Varvara Trachana
Summary: Research shows that oxidative stress can lead to upregulation, phosphorylation, and nuclear translocation of Cav-1 in young stem cells, but this regulation is lost as cells age. Older cells are unable to repair DNA damage, and downregulation of Cav-1 results in persistent DNA damage and onset of senescence. Additionally, the establishment of senescence is mediated by autophagy activation.
Review
Pharmacology & Pharmacy
Shilu Luo, Ming Yang, Hao Zhao, Yachun Han, Na Jiang, Jinfei Yang, Wei Chen, Chenrui Li, Yan Liu, Chanyue Zhao, Lin Sun
Summary: Caveolin-1 (Cav-1) plays a crucial role in regulating cellular endocytosis, stress responses, and signal transduction. It is involved in mediating the endocytosis of albumin, cholesterol, and glucose, participating in cellular metabolic reprogramming, and contributing to the progression of kidney disease. Cav-1 also serves as a potential therapeutic target for the treatment of kidney disease.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Food Science & Technology
Ivan Cruz-Chamorro, Nuria Alvarez-Sanchez, Ana Isabel Alvarez-Rios, Guillermo Santos-Sanchez, Justo Pedroche, Francisco Millan, Cecilio Carrera Sanchez, Maria Soledad Fernandez-Pachon, Maria Carmen Millan-Linares, Alicia Martinez-Lopez, Patricia Judith Lardone, Ignacio Bejarano, Juan Miguel Guerrero, Antonio Carrillo-Vico
Summary: This study aimed to evaluate the safety and efficacy of a beverage containing Lupinus angustifolius protein hydrolysates (LPHs) on the immune, oxidative, and metabolic status of healthy subjects. The results showed that LPHb ingestion was safe and effective in enhancing the anti-/pro-inflammatory response of PBMCs and improving cellular antioxidant capacity. Additionally, LPHb was found to reduce the LDL-C/HDL-C atherogenic index and serum total cholesterol levels, especially in the male cohort.
MOLECULAR NUTRITION & FOOD RESEARCH
(2021)
Article
Cell Biology
Shanshan Wang, Taiga Ichinomiya, Yuki Terada, Dongsheng Wang, Hemal H. Patel, Brian P. Head
Summary: Mitochondrial dysfunction is a pivotal factor in Alzheimer's Disease, and the protein Cav-1 may play a critical role in maintaining normal mitochondrial morphology and function by regulating mitochondrial dynamics. Neuron-targeted expression of Cav-1 in PSAPP mice was shown to improve cognitive function, neuronal morphology, and synaptic structure, while also protecting mitochondrial function.
Article
Immunology
Dupiao Zhang, Chen Jin, Tao Han, Jianpeng Chen, Mazhar Ali Raza, Baolong Li, Liang Wang, Hede Yan
Summary: Random flaps are commonly used to cover large skin defects and surgical tissue reconstructions, but their clinical application is limited due to flap necrosis. Sinomenine has been found to enhance flap survival by reducing oxidative stress, promoting autophagy, and angiogenesis. The mechanism involves the PI3K/AKT signaling pathway, antioxidant activity, and eNOS system.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Zhao Chen, Zhecheng Wang, Deshun Liu, Xuzi Zhao, Shili Ning, Xingming Liu, Guangzhi Wang, Feng Zhang, Fuwen Luo, Jihong Yao, Xiaofeng Tian
Summary: This study found that caveolin-1 (Cav1) plays a critical role in protecting against intestinal ischemia reperfusion (I/R) injury by regulating protein kinase C beta II (PKC beta II) inactivation. Inhibition of Cav1 resulted in excessive PKC beta II activation and worsened intestinal injury. This finding offers a new therapeutic strategy for the prevention and treatment of intestinal I/R injury.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Review
Biochemistry & Molecular Biology
Colin J. Barnstable, Mingliang Zhang, Joyce Tombran-Tink
Summary: Most major retinal degenerative diseases are linked to oxidative stress, with mitochondria being a major contributor through the generation of reactive oxygen species (ROS). UCP2, a member of the uncoupling protein family, can modulate ROS production by regulating the proton gradient across the inner mitochondrial membrane. Control of UCP2 expression and activity at multiple levels makes it a promising candidate for therapeutic intervention.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Medicine, General & Internal
Guang-Hui Deng, Chao-Feng Wu, Yun-Jia Li, Hao Shi, Wei-Chao Zhong, Mu-Keng Hong, Jun-Jie Li, Jia-Min Zhao, Chang Liu, Meng-Chen Qin, Zhi-Yun Zeng, Wei-Min Zhang, Ken Kin Lam Yung, Zhi-Ping Lv, Lei Gao
Summary: This study confirms that Cav-1 is a key protein that regulates iron and lipid metabolism homeostasis. It plays a crucial role in predicting and protecting against the development of NAFLD.
MILITARY MEDICAL RESEARCH
(2023)
Article
Biotechnology & Applied Microbiology
Liyuan Zhou, Changchen Hu, Yujun Li, Binquan Wang
Summary: This study investigated the therapeutic effect of Sulforaphane (SFP) on hypoxic vestibular vertigo (HVV) using a rat model. The results showed that SFP treatment helped to maintain the balance of escape latency and concentrations of nitric oxide (NO), glutathione (GSH) and superoxide dismutase (SOD), and restored the inhibited expression of NRF2. SFP treatment also increased the production of NO and cyclic guanosine monophosphate (cGMP) in a dose-dependent manner.
Article
Biochemistry & Molecular Biology
Sheng-Qing Gao, Jia-Jun Shi, Shu-Hao Miao, Tao Li, Chao-Chao Gao, Yan-Ling Han, Jia-Yin Qiu, Yun-Song Zhuang, Meng-Liang Zhou
Summary: This study investigated the contribution of the interaction between endothelial NOX4 and DHFR to eNOS uncoupling after SAH. Inhibiting endothelial NOX4 and increasing endothelial DHFR levels alleviated eNOS uncoupling and improved neurological function after SAH.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)