scholarly journals Integrin-α9β1 as a Novel Therapeutic Target for Refractory Diseases: Recent Progress and Insights

2021 ◽  
Vol 12 ◽  
Author(s):  
Shihan Xu ◽  
Tingwei Zhang ◽  
Zhengguo Cao ◽  
Wenjie Zhong ◽  
Chuangwei Zhang ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Recent Progress ◽  
Molecular Mechanisms ◽  
Physiological State ◽  
Molecular Signals ◽  
Complex Signaling ◽  
Refractory Diseases ◽  
Integrin Family ◽  
Novel Therapeutic

Integrins refer to heterodimers consisting of subunits α and β. They serve as receptors on cell membranes and interact with extracellular ligands to mediate intracellular molecular signals. One of the least-studied members of the integrin family is integrin-α9β1, which is widely distributed in various human tissues and organs. Integrin-α9β1 regulates the physiological state of cells through a variety of complex signaling pathways to participate in the specific pathological processes of some intractable diseases. In recent years, an increasing amount of research has focused on the role of α9β1 in the molecular mechanisms of different refractory diseases and its promising potential as a therapeutic target. Accordingly, this review introduces and summarizes recent research related to integrin-α9β1, describes the synergistic functions of α9β1 and its corresponding ligands in cancer, autoimmune diseases, nerve injury and thrombosis and, more importantly, highlights the potential of α9β1 as a distinctive target for the treatment of these intractable diseases.

Molecular Interactions of α-Synuclein, Mitochondria, and Cellular Degradation Pathways in Parkinson's Disease

2020 ◽  
pp. 212-234
Author(s):  
Mansi Verma ◽  
Sujata Basu ◽  
Manisha Singh ◽  
Rachana R. ◽  
Simrat Kaur ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Interactions ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Degradation Pathways ◽  
Functional Changes ◽  
The World ◽  
Novel Therapeutic

Parkinson's disease (PD) has been reported to be the most common neurodegenerative diseases all over the world. Several proteins are associated and responsible for causing PD. One such protein is α-synuclein. This chapter discusses the role of α-synuclein in PD. Various genetic and epigenetic factors, which cause structural and functional changes for α-synuclein, have been described. Several molecular mechanisms, which are involved in regulating mitochondrial and lysosomal related pathways and are linked to α-synuclein, have been discussed in detail. The knowledge gathered is further discussed in terms of using α-synuclein as a diagnostic marker for PD and as a novel therapeutic target for the same.

Abstract 533: Crucial Role of Rho-Kinase in Pressure Overload--Induced Right Ventricular Hypertrophy and Dysfunction in Mice: A Possible Novel Therapeutic Target of Right Ventricular Failure

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Shohei Ikeda ◽  
Kimio Satoh ◽  
Nobuhiro Kikuchi ◽  
Satoshi Miyata ◽  
Kota Suzuki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Right Ventricular ◽  
Therapeutic Target ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Rho Kinase ◽  
Pressure Overload ◽  
Dominant Negative ◽  
Term Survival ◽  
Novel Therapeutic

Rationale: Right ventricular (RV) failure is the leading cause of death in various cardiopulmonary diseases, including pulmonary hypertension. It is generally considered that the RV is vulnerable to pressure-overload as compared with the left ventricle (LV). However, as compared with LV failure, the molecular mechanisms of RV failure are poorly understood. Objective: We aimed to identify molecular therapeutic targets for RV failure in a mouse model of pressure-overload. Methods and Results: To induce pressure-overload to respective ventricles, we performed pulmonary artery constriction (PAC) or transverse aortic constriction (TAC) in mice. We first performed microarray analysis and found that the molecules related to RhoA/Rho-kinase and integrin pathways were significantly up-regulated in the RV with PAC compared with the LV with TAC. Then, we examined the responses of both ventricles to chronic pressure-overload in vivo. We demonstrated that compared with TAC, PAC caused greater extents of mortality, Rho-kinase expression (especially ROCK2 isoform) and oxidative stress in pressure-overloaded RV, reflecting the weakness of the RV in response to pressure-overload. Additionally, mechanical stretch of RV cardiomyocytes from rats immediately up-regulated ROCK2 expression (not ROCK1), suggesting the specific importance of ROCK2 in stretch-induced responses of RV tissues. Furthermore, mice with myocardial-specific overexpression of dominant-negative Rho-kinase (DN-RhoK) showed resistance to pressure-overload-induced hypertrophy and dysfunction associated with reduced oxidative stress. Finally, DN-RhoK mice showed a significantly improved long-term survival in both PAC and TAC as compared with littermate controls. Conclusions: These results indicate that the Rho-kinase pathway plays a crucial role in RV hypertrophy and dysfunction, suggesting that the pathway is a novel therapeutic target of RV failure in humans.

scholarly journals Role of Dimerized C16orf74 in Aggressive Pancreatic Cancer: A Novel Therapeutic Target

2019 ◽  
Vol 19 (1) ◽  
pp. 187-198 ◽  
Author(s):  
Toshihiro Kushibiki ◽  
Toru Nakamura ◽  
Masumi Tsuda ◽  
Takahiro Tsuchikawa ◽  
Koji Hontani ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Therapeutic Target ◽  
Novel Therapeutic

scholarly journals The Role of DLLs in Cancer: A Novel Therapeutic Target

2020 ◽  
Vol Volume 13 ◽  
pp. 3881-3901 ◽  
Author(s):  
Meng-Xi Xiu ◽  
Yuan-Meng Liu ◽  
Bo-hai Kuang
Keyword(s):  
Therapeutic Target ◽  
Novel Therapeutic

Update on the role of autophagy in systemic lupus erythematosus: A novel therapeutic target

2015 ◽  
Vol 71 ◽  
pp. 190-193 ◽  
Author(s):  
Qingjun Pan ◽  
Caina Gao ◽  
Yanwen Chen ◽  
Yongmin Feng ◽  
Wei Jing Liu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Therapeutic Target ◽  
Systemic Lupus ◽  
Novel Therapeutic

scholarly journals Role of acidic tumor microenvironment in tumor pathogenesis and targeting

2020 ◽  
pp. 34-40
Author(s):  
Vishal Sharma ◽  
Chhaya Bawa ◽  
Kuldeep Chand Vatsyan
Keyword(s):  
Cell Growth ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Physiological State ◽  
Therapeutic Interventions ◽  
Cancer Cell Growth ◽  
Molecular Alterations ◽  
Cancer Pathogenesis

Extensive efforts are going on to understand the molecular mechanisms behind tumor initiation, progression, and invasion and find novel targets for cancer treatment. The physiological state of the tumor microenvironment (TME) is crucial to every step of tumor cell growth and angiogenesis. Cancer cells are rarely in contact with each other. The intervening medium between the cancer cells, immune cells, and other cells become acidic, which significantly affects cancer pathogenesis. It could be a novel targeting marker and may help treat tumors. Even after extensive research in this area, the nature of molecular alterations and the basic mechanisms in the tumor microenvironment remains unclear. Based on recent studies of TME, this mini-review bids a more inclusive overview of the role of TME in cancer cell growth. Also, it helps to understand the potential of TME for therapeutic interventions.

scholarly journals The Role of Altered Mitochondrial Metabolism in Thyroid Cancer Development and Mitochondria-Targeted Thyroid Cancer Treatment

2021 ◽  
Vol 23 (1) ◽  
pp. 460
Author(s):  
Siarhei A. Dabravolski ◽  
Nikita G. Nikiforov ◽  
Alexander D. Zhuravlev ◽  
Nikolay A. Orekhov ◽  
Liudmila M. Mikhaleva ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Energy Production ◽  
Recent Progress ◽  
Molecular Mechanisms ◽  
Reactive Oxygen Species Generation ◽  
Common Type ◽  
Mitochondrial Metabolism ◽  
Oxygen Species ◽  
Tumour Formation

Thyroid cancer (TC) is the most common type of endocrine malignancy. Tumour formation, progression, and metastasis greatly depend on the efficacy of mitochondria—primarily, the regulation of mitochondria-mediated apoptosis, Ca2+ homeostasis, dynamics, energy production, and associated reactive oxygen species generation. Recent studies have successfully confirmed the mitochondrial aetiology of thyroid carcinogenesis. In this review, we focus on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism. We also discuss the repurposing of known drugs and the induction of mitochondria-mediated apoptosis as a new trend in the development of anti-TC therapy.

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