scholarly journals Statement of Retraction: β-Adrenergic receptor structure and function: molecular insights guiding the development of novel therapeutic strategies to treat malignancy

2021 ◽  
pp. 1-1
Keyword(s):  
Adrenergic Receptor ◽  
Therapeutic Strategies ◽  
Structure And Function ◽  
Receptor Structure ◽  
Novel Therapeutic Strategies ◽  
And Function ◽  
Novel Therapeutic

scholarly journals β-Adrenergic Receptor Blockers Restore Cardiac Calcium Release Channel (Ryanodine Receptor) Structure and Function in Heart Failure

Circulation ◽  
2001 ◽  
Vol 104 (23) ◽  
pp. 2843-2848 ◽  
Author(s):  
Steven Reiken ◽  
Marta Gaburjakova ◽  
Jana Gaburjakova ◽  
Kun-lun He ◽  
Alfonso Prieto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ryanodine Receptor ◽  
Adrenergic Receptor ◽  
Calcium Release ◽  
Structure And Function ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Receptor Structure ◽  
Receptor Blockers ◽  
And Function

scholarly journals Glioma Stem-Like Cells and Metabolism: Potential for Novel Therapeutic Strategies

2021 ◽  
Vol 11 ◽  
Author(s):  
Abigail Harland ◽  
Xia Liu ◽  
Mattia Ghirardello ◽  
M. Carmen Galan ◽  
Claire M. Perks ◽  
...  
Keyword(s):  
Therapeutic Approach ◽  
Therapeutic Strategies ◽  
Tumour Bulk ◽  
Novel Therapeutic Strategies ◽  
And Function ◽  
Novel Therapeutic

Glioma stem-like cells (GSCs) were first described as a population which may in part be resistant to traditional chemotherapeutic therapies and responsible for tumour regrowth. Knowledge of the underlying metabolic complexity governing GSC growth and function may point to potential differences between GSCs and the tumour bulk which could be harnessed clinically. There is an increasing interest in the direct/indirect targeting or reprogramming of GSC metabolism as a potential novel therapeutic approach in the adjuvant or recurrent setting to help overcome resistance which may be mediated by GSCs. In this review we will discuss stem-like models, interaction between metabolism and GSCs, and potential current and future strategies for overcoming GSC resistance.

scholarly journals TFEB Biology and Agonists at a Glance

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 333
Author(s):  
Mingyue Chen ◽  
Yashuang Dai ◽  
Siyu Liu ◽  
Yuxin Fan ◽  
Zongxian Ding ◽  
...  
Keyword(s):  
Transcriptional Regulator ◽  
Therapeutic Strategies ◽  
Disease Models ◽  
Cellular Survival ◽  
Promising Strategy ◽  
Pathogenic Factors ◽  
Transcription Factor Eb ◽  
Novel Therapeutic Strategies ◽  
And Function ◽  
Novel Therapeutic

Autophagy is a critical regulator of cellular survival, differentiation, development, and homeostasis, dysregulation of which is associated with diverse diseases including cancer and neurodegenerative diseases. Transcription factor EB (TFEB), a master transcriptional regulator of autophagy and lysosome, can enhance autophagic and lysosomal biogenesis and function. TFEB has attracted a lot of attention owing to its ability to induce the intracellular clearance of pathogenic factors in a variety of disease models, suggesting that novel therapeutic strategies could be based on the modulation of TFEB activity. Therefore, TFEB agonists are a promising strategy to ameliorate diseases implicated with autophagy dysfunction. Recently, several TFEB agonists have been identified and preclinical or clinical trials are applied. In this review, we present an overview of the latest research on TFEB biology and TFEB agonists.

PCSK9 Inhibitors: Novel Therapeutic Strategies for Lowering LDLCholesterol

2018 ◽  
Vol 19 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Yan Wang ◽  
Zhao-Peng Liu
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Maximum Tolerated Dose ◽  
Therapeutic Strategies ◽  
Low Density ◽  
Pcsk9 Inhibitors ◽  
Cvd Risk ◽  
Safety Issues ◽  
Novel Therapeutic Strategies ◽  
Novel Therapeutic

Statins are currently the major therapeutic strategies to lower low-density lipoprotein cholesterol (LDL-C) levels. However, a number of hypercholesterolemia patients still have a residual cardiovascular disease (CVD) risk despite taking the maximum-tolerated dose of statins. Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low-density lipoprotein receptor (LDLR), inducing its degradation in the lysosome and inhibiting LDLR recirculating to the cell membranes. The gain-offunction mutations in PCSK9 elevate the LDL-C levels in plasma. Therefore, PCSK9 inhibitors become novel therapeutic approaches in the treatment of hypercholesterolemia. Several PCSK9 inhibitors have been under investigation, and much progress has been made in clinical trials, especially for monoclonal antibodies (MoAbs). Two MoAbs, evolocumab and alirocumab, are now in clinical use. In this review, we summarize the development of PCSK9 inhibitors, including antisense oligonucleotides (ASOs), small interfering RNA (siRNA), small molecule inhibitor, MoAbs, mimetic peptides and adnectins, and the related safety issues.

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