scholarly journals Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Wei-Xing Ma ◽  
Chun-Yan Li ◽  
Ran Tao ◽  
Xin-Ping Wang ◽  
Liang-Jun Yan
Keyword(s):  
Mitochondrial Dysfunction ◽  
Reducing Power ◽  
Therapeutic Approaches ◽  
Heart Damage ◽  
The Past ◽  
Reductive Stress ◽  
Developing Heart ◽  
Disease Induction ◽  
Risk Assessment And Prevention ◽  
Underlying Mechanisms

The goal of this review was to summarize reported studies focusing on cellular reductive stress-induced mitochondrial dysfunction, cardiomyopathy, dithiothreitol- (DTT-) induced reductive stress, and reductive stress-related free radical reactions published in the past five years. Reductive stress is considered to be a double-edged sword in terms of antioxidation and disease induction. As many underlying mechanisms are still unclear, further investigations are obviously warranted. Nonetheless, reductive stress is thought to be caused by elevated levels of cellular reducing power such as NADH, glutathione, and NADPH; and this area of research has attracted increasing attention lately. Albeit, we think there is a need to conduct further studies in identifying more indicators of the risk assessment and prevention of developing heart damage as well as exploring more targets for cardiomyopathy treatment. Hence, it is expected that further investigation of underlying mechanisms of reductive stress-induced mitochondrial dysfunction will provide novel insights into therapeutic approaches for ameliorating reductive stress-induced cardiomyopathy.

Autoimmune-mediated renal disease and hypertension

2021 ◽  
Vol 135 (17) ◽  
pp. 2165-2196
Author(s):  
Erika I. Boesen ◽  
Rahul M. Kakalij
Keyword(s):  
Renal Disease ◽  
Lupus Erythematosus ◽  
Functional Decline ◽  
Immunoglobulin A ◽  
Renal Diseases ◽  
Therapeutic Approaches ◽  
The Past ◽  
Current State ◽  
Underlying Mechanisms ◽  
Disease Specific

Abstract Hypertension is a major risk factor for cardiovascular disease, chronic kidney disease (CKD), and mortality. Troublingly, hypertension is highly prevalent in patients with autoimmune renal disease and hastens renal functional decline. Although progress has been made over the past two decades in understanding the inflammatory contributions to essential hypertension more broadly, the mechanisms active in autoimmune-mediated renal diseases remain grossly understudied. This Review provides an overview of the pathogenesis of each of the major autoimmune diseases affecting the kidney that are associated with hypertension, and describes the current state of knowledge regarding hypertension in these diseases and their management. Specifically, discussion focuses on Systemic Lupus Erythematosus (SLE) and Lupus Nephritis (LN), Immunoglobulin A (IgA) Nephropathy, Idiopathic Membranous Nephropathy (IMN), Anti-Neutrophil Cytoplasmic Antibody (ANCA)-associated glomerulonephritis, and Thrombotic Thrombocytopenic Purpura (TTP). A summary of disease-specific animal models found to exhibit hypertension is also included to highlight opportunities for much needed further investigation of underlying mechanisms and novel therapeutic approaches.

Novel Findings of Anti-cancer Property of Propofol

2018 ◽  
Vol 18 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Jiaqiang Wang ◽  
Chien-shan Cheng ◽  
Yan Lu ◽  
Xiaowei Ding ◽  
Minmin Zhu ◽  
...  
Keyword(s):  
General Anesthesia ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Intravenous Anesthetic ◽  
The Past ◽  
Anti Cancer ◽  
Underlying Mechanisms ◽  
Recent Attention

Background: Propofol, a widely used intravenous anesthetic agent, is traditionally applied for sedation and general anesthesia. Explanation: Recent attention has been drawn to explore the effect and mechanisms of propofol against cancer progression in vitro and in vivo. Specifically, the proliferation-inhibiting and apoptosis-inducing properties of propofol in cancer have been studied. However, the underlying mechanisms remain unclear. Conclusion: This review focused on the findings within the past ten years and aimed to provide a general overview of propofol's malignance-modulating properties and the potential molecular mechanisms.

scholarly journals Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Zhimin Zhang ◽  
Congying Wei ◽  
Yanfen Zhou ◽  
Tao Yan ◽  
Zhengqiang Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Umbilical Vein ◽  
Dependent Manner ◽  
Human Umbilical Vein ◽  
Homologous Protein ◽  
Intracellular Ros ◽  
Underlying Mechanisms ◽  
Umbilical Vein Endothelial Cells

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspase-3. Prolonged Hcy treatment also upregulated glucose-regulated protein 78 (GRP78), activated protein kinase RNA-like ER kinase (PERK), and induced the expression of C/EBP homologous protein (CHOP) and the phosphorylation of NF-κb. The inhibition of NOX4 decreased the production of ROS and alleviated the Hcy-induced HUVEC apoptosis and ER stress. Blocking the PERK pathway partly alleviated Hcy-induced HUVEC apoptosis and the activation of NF-κb. Taken together, our results suggest that Hcy-induced mitochondrial dysfunction crucially modulated apoptosis and contributed to the activation of ER stress in HUVEC. The excessive activation of the PERK pathway partly contributed to Hcy-induced HUVEC apoptosis and the phosphorylation of NF-κb.

Exercise Physiology From 1980 to 2020: Application of the Natural Sciences

2021 ◽  
pp. 1-10
Author(s):  
Jane A. Kent ◽  
Kate L. Hayes
Keyword(s):  
Human Performance ◽  
Exercise Physiology ◽  
Natural Sciences ◽  
The Past ◽  
Interdisciplinary Field ◽  
Advanced Technologies ◽  
Health And Disease ◽  
Fundamental Research ◽  
Research Questions ◽  
Underlying Mechanisms

The field of exercise physiology has enjoyed tremendous growth in the past 40 years. With its foundations in the natural sciences, it is an interdisciplinary field that is highly relevant to human performance and health. The focus of this review is on highlighting new approaches, knowledge, and opportunities that have emerged in exercise physiology over the last four decades. Key among these is the adoption of advanced technologies by exercise physiologists to address fundamental research questions, and the expansion of research topics to range from molecular to organismal, and population scales in order to clarify the underlying mechanisms and impact of physiological responses to exercise in health and disease. Collectively, these advances have ensured the position of the field as a partner in generating new knowledge across many scientific and health disciplines.

scholarly journals Antioxidant treatment induces reductive stress associated with mitochondrial dysfunction in adipocytes

2018 ◽  
Vol 294 (7) ◽  
pp. 2340-2352 ◽  
Author(s):  
Eduard Peris ◽  
Peter Micallef ◽  
Alexandra Paul ◽  
Vilborg Palsdottir ◽  
Annika Enejder ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Antioxidant Treatment ◽  
Reductive Stress

Underlying mechanisms and chemical/biochemical therapeutic approaches to ameliorate protein misfolding neurodegenerative diseases

BioFactors ◽  
2016 ◽  
Vol 43 (6) ◽  
pp. 737-759 ◽  
Author(s):  
Seyedhossein Hekmatimoghaddam ◽  
Mohamad Reza Zare-Khormizi ◽  
Fatemeh Pourrajab
Keyword(s):  
Neurodegenerative Diseases ◽  
Protein Misfolding ◽  
Therapeutic Approaches ◽  
Underlying Mechanisms

You Are What You Feed

2021 ◽  
Author(s):  
Angela Duckworth ◽  
Keyword(s):  
Therapeutic Approaches ◽  
The Past ◽  
Cash Register

In one of Tim Beck's recent articles, he tells the story of David, a 37-year-old man hospitalized with a diagnosis of schizophrenia.  David's symptoms are severe, and traditional therapeutic approaches have so far been unsuccessful. Some days it's a challenge for him to even engage in a conversation. One day, his therapist asks him what activity he liked most in the past. “McDonald's,” he replies. “I've always enjoyed going to McDonald's for a hamburger.” The therapist proposes that they walk over to the hospital restaurant. On arrival, without explanation, a miraculous transformation occurs. Suddenly, David is alert to his surroundings, able to cheerfully complete the transaction at the cash register and even to joke with the cashier before taking his food. 

scholarly journals Mitochondrial Dysfunction in Obesity and Reproduction

Endocrinology ◽  
2020 ◽  
Vol 162 (1) ◽  
Author(s):  
Manasi Das ◽  
Consuelo Sauceda ◽  
Nicholas J G Webster
Keyword(s):  
Mitochondrial Dysfunction ◽  
Energy Production ◽  
Molecular Mechanisms ◽  
Human Populations ◽  
Metabolic Alterations ◽  
Genetic Manipulations ◽  
The Past ◽  
Calcium Buffering

Abstract Mounting evidence suggests a role for mitochondrial dysfunction in the pathogenesis of many diseases, including type 2 diabetes, aging, and ovarian failure. Because of the central role of mitochondria in energy production, heme biosynthesis, calcium buffering, steroidogenesis, and apoptosis signaling within cells, understanding the molecular mechanisms behind mitochondrial dysregulation and its potential implications in disease is critical. This review will take a journey through the past and summarize what is known about mitochondrial dysfunction in various disorders, focusing on metabolic alterations and reproductive abnormalities. Evidence is presented from studies in different human populations, and rodents with genetic manipulations of pathways known to affect mitochondrial function.

scholarly journals Molecular Mechanisms of Heat Shock Factors in Cancer

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1202
Author(s):  
Mikael Christer Puustinen ◽  
Lea Sistonen
Keyword(s):  
Heat Shock ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Heat Shock Factors ◽  
Therapeutic Approaches ◽  
The Past ◽  
Cancer Types ◽  
Cellular Pathways ◽  
As Stress ◽  
Regulatory Functions

Malignant transformation is accompanied by alterations in the key cellular pathways that regulate development, metabolism, proliferation and motility as well as stress resilience. The members of the transcription factor family, called heat shock factors (HSFs), have been shown to play important roles in all of these biological processes, and in the past decade it has become evident that their activities are rewired during tumorigenesis. This review focuses on the expression patterns and functions of HSF1, HSF2, and HSF4 in specific cancer types, highlighting the mechanisms by which the regulatory functions of these transcription factors are modulated. Recently developed therapeutic approaches that target HSFs are also discussed.

scholarly journals Cellular Stress in the Pathogenesis of Muscular Disorders—From Cause to Consequence

2020 ◽  
Vol 21 (16) ◽  
pp. 5830 ◽  
Author(s):  
Alexander Mensch ◽  
Stephan Zierz
Keyword(s):  
Stress Response ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
Therapeutic Approaches ◽  
Muscular Disorders ◽  
Adaptive Mechanisms ◽  
Relevant Role ◽  
Pathogenetic Factor ◽  
Underlying Mechanisms

Cellular stress has been considered a relevant pathogenetic factor in a variety of human diseases. Due to its primary functions by means of contractility, metabolism, and protein synthesis, the muscle cell is faced with continuous changes of cellular homeostasis that require rapid and coordinated adaptive mechanisms. Hence, a prone susceptibility to cellular stress in muscle is immanent. However, studies focusing on the cellular stress response in muscular disorders are limited. While in recent years there have been emerging indications regarding a relevant role of cellular stress in the pathophysiology of several muscular disorders, the underlying mechanisms are to a great extent incompletely understood. This review aimed to summarize the available evidence regarding a deregulation of the cellular stress response in individual muscle diseases. Potential mechanisms, as well as involved pathways are critically discussed, and respective disease models are addressed. Furthermore, relevant therapeutic approaches that aim to abrogate defects of cellular stress response in muscular disorders are outlined.

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