scholarly journals Autophagy and pancreatitis

2012 ◽  
Vol 303 (9) ◽  
pp. G993-G1003 ◽  
Author(s):  
Anna S. Gukovskaya ◽  
Ilya Gukovsky
Keyword(s):  
Acute Pancreatitis ◽  
Strong Evidence ◽  
Inflammatory Disease ◽  
Exocrine Pancreas ◽  
Molecular Targets ◽  
Therapeutic Strategies ◽  
Experimental Models ◽  
Degradative Pathway ◽  
Considerable Morbidity ◽  
Insight Into

Acute pancreatitis is an inflammatory disease of the exocrine pancreas that carries considerable morbidity and mortality; its pathophysiology remains poorly understood. Recent findings from experimental models and genetically altered mice summarized in this review reveal that autophagy, the principal cellular degradative pathway, is impaired in pancreatitis and that one cause of autophagy impairment is defective function of lysosomes. We propose that the lysosomal/autophagic dysfunction is a key initiating event in pancreatitis and a converging point of multiple deranged pathways. There is strong evidence supporting this hypothesis. Investigation of autophagy in pancreatitis has just started, and many questions about the “upstream” mechanisms mediating the lysosomal/autophagic dysfunction and the “downstream” links to pancreatitis pathologies need to be explored. Answers to these questions should provide insight into novel molecular targets and therapeutic strategies for treatment of pancreatitis.

scholarly journals Experimental Models of Sarcopenia: Bridging Molecular Mechanism and Therapeutic Strategy

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1385 ◽  
Author(s):  
Sakulrat Mankhong ◽  
Sujin Kim ◽  
Sohee Moon ◽  
Hyo-Bum Kwak ◽  
Dong-Ho Park ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Functional Disability ◽  
Molecular Targets ◽  
Therapeutic Strategies ◽  
Experimental Models ◽  
Current Status ◽  
Drug Candidates ◽  
Novel Therapeutic Strategies

Sarcopenia has been defined as a progressive decline of skeletal muscle mass, strength, and functions in elderly people. It is accompanied by physical frailty, functional disability, falls, hospitalization, and mortality, and is becoming a major geriatric disorder owing to the increasing life expectancy and growing older population worldwide. Experimental models are critical to understand the pathophysiology of sarcopenia and develop therapeutic strategies. Although its etiologies remain to be further elucidated, several mechanisms of sarcopenia have been identified, including cellular senescence, proteostasis imbalance, oxidative stress, and “inflammaging.” In this article, we address three main aspects. First, we describe the fundamental aging mechanisms. Next, we discuss both in vitro and in vivo experimental models based on molecular mechanisms that have the potential to elucidate the biochemical processes integral to sarcopenia. The use of appropriate models to reflect sarcopenia and/or its underlying pathways will enable researchers to understand sarcopenia and develop novel therapeutic strategies for sarcopenia. Lastly, we discuss the possible molecular targets and the current status of drug candidates for sarcopenia treatment. In conclusion, the development of experimental models for sarcopenia is essential to discover molecular targets that are valuable as biochemical biomarkers and/or therapeutic targets for sarcopenia.

scholarly journals Obesity causes PGC-1α deficiency in exocrine pancreas leading to IL-6 upregulation via NF-κB in acute pancreatitis

2021 ◽  
Vol 165 ◽  
pp. 36
Author(s):  
Sergio Rius-Pérez ◽  
Salvador Pérez ◽  
Pablo Martí-Andrés ◽  
Isabela Finamor ◽  
Ignacio Prieto ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Exocrine Pancreas

scholarly journals Superhydrophobic Nanocoatings as Intervention against Biofilm-Associated Bacterial Infections

Nanomaterials ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 1046
Author(s):  
Yinghan Chan ◽  
Xun Hui Wu ◽  
Buong Woei Chieng ◽  
Nor Azowa Ibrahim ◽  
Yoon Yee Then
Keyword(s):  
Biofilm Formation ◽  
Bacterial Infections ◽  
Therapeutic Strategies ◽  
Public Healthcare ◽  
Persistent Infections ◽  
Promising Strategy ◽  
Antimicrobial Interventions ◽  
Novel Therapeutic Strategies ◽  
Insight Into ◽  
Microbial Attachment

Biofilm formation represents a significant cause of concern as it has been associated with increased morbidity and mortality, thereby imposing a huge burden on public healthcare system throughout the world. As biofilms are usually resistant to various conventional antimicrobial interventions, they may result in severe and persistent infections, which necessitates the development of novel therapeutic strategies to combat biofilm-based infections. Physicochemical modification of the biomaterials utilized in medical devices to mitigate initial microbial attachment has been proposed as a promising strategy in combating polymicrobial infections, as the adhesion of microorganisms is typically the first step for the formation of biofilms. For instance, superhydrophobic surfaces have been shown to possess substantial anti-biofilm properties attributed to the presence of nanostructures. In this article, we provide an insight into the mechanisms underlying biofilm formation and their composition, as well as the applications of nanomaterials as superhydrophobic nanocoatings for the development of novel anti-biofilm therapies.

scholarly journals Ca 2+ toxicity and mitochondrial damage in acute pancreatitis: translational overview

2016 ◽  
Vol 371 (1700) ◽  
pp. 20150425 ◽  
Author(s):  
József Maléth ◽  
Péter Hegyi
Keyword(s):  
Acute Pancreatitis ◽  
Mitochondrial Permeability Transition ◽  
Clinical Investigation ◽  
Cell Damage ◽  
Specific Treatment ◽  
Experimental Models ◽  
Mitochondrial Damage ◽  
Cell Functions ◽  
Cellular Ca

Acute pancreatitis (AP) is a leading cause of hospitalization among non-malignant gastrointestinal disorders. The mortality of severe AP can reach 30–50%, which is most probably owing to the lack of specific treatment. Therefore, AP is a major healthcare problem, which urges researchers to identify novel drug targets. Studies from the last decades highlighted that the toxic cellular Ca 2+ overload and mitochondrial damage are key pathogenic steps in the disease development affecting both acinar and ductal cell functions. Moreover, recent observations showed that modifying the cellular Ca 2+ signalling might be beneficial in AP. The inhibition of Ca 2+ release from the endoplasmic reticulum or the activity of plasma membrane Ca 2+ influx channels decreased the severity of AP in experimental models. Similarly, inhibition of mitochondrial permeability transition pore (MPTP) opening also seems to improve the outcome of AP in in vivo animal models. At the moment MPTP blockers are under detailed clinical investigation to test whether interventions in MPTP openings and/or Ca 2+ homeostasis of the cells can be specific targets in prevention or treatment of cell damage in AP. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.

Nuclear receptor Nur77: its role in chronic inflammatory diseases

2021 ◽  
Author(s):  
Sanne C. Lith ◽  
Carlie J.M. de Vries
Keyword(s):  
Nuclear Receptor ◽  
Inflammatory Disease ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Alternative Mechanism ◽  
Signaling Complex

Abstract Nur77 is a nuclear receptor that has been implicated as a regulator of inflammatory disease. The expression of Nur77 increases upon stimulation of immune cells and is differentially expressed in chronically inflamed organs in human and experimental models. Furthermore, in a variety of animal models dedicated to study inflammatory diseases, changes in Nur77 expression alter disease outcome. The available studies comprise a wealth of information on the function of Nur77 in diverse cell types and tissues. Negative cross-talk of Nur77 with the NFκB signaling complex is an example of Nur77 effector function. An alternative mechanism of action has been established, involving Nur77-mediated modulation of metabolism in macrophages as well as in T cells. In this review, we summarize our current knowledge on the role of Nur77 in atherosclerosis, inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis, and sepsis. Detailed insight in the control of inflammatory responses will be essential in order to advance Nur77-targeted therapeutic interventions in inflammatory disease.

scholarly journals Skin and Gut Microbiome in Psoriasis: Gaining Insight Into the Pathophysiology of It and Finding Novel Therapeutic Strategies

2020 ◽  
Vol 11 ◽  
Author(s):  
Lihui Chen ◽  
Jie Li ◽  
Wu Zhu ◽  
Yehong Kuang ◽  
Tao Liu ◽  
...  
Keyword(s):  
Therapeutic Strategy ◽  
Therapeutic Strategies ◽  
Intestinal Microbiome ◽  
Core Microbiome ◽  
The Core ◽  
The World ◽  
Novel Therapeutic Strategies ◽  
Insight Into ◽  
Gaining Insight

Psoriasis affects the health of myriad populations around the world. The pathogenesis is multifactorial, and the exact driving factor remains unclear. This condition arises from the interaction between hyperproliferative keratinocytes and infiltrating immune cells, with poor prognosis and high recurrence. Better clinical treatments remain to be explored. There is much evidence that alterations in the skin and intestinal microbiome play an important role in the pathogenesis of psoriasis, and restoration of the microbiome is a promising preventive and therapeutic strategy for psoriasis. Herein, we have reviewed recent studies on the psoriasis-related microbiome in an attempt to confidently identify the “core” microbiome of psoriasis patients, understand the role of microbiome in the pathogenesis of psoriasis, and explore new therapeutic strategies for psoriasis through microbial intervention.

scholarly journals Erratum: Corrigendum: Experimental Models in Syrian Golden Hamster Replicate Human Acute Pancreatitis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yunan Wang ◽  
Abudurexiti Kayoumu ◽  
Guotao Lu ◽  
Pengfei Xu ◽  
Xu Qiu ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Golden Hamster ◽  
Experimental Models ◽  
Syrian Golden Hamster ◽  
Human Acute Pancreatitis

Effects of tetraprenylacetone on pancreatic exocrine secretion and acute pancreatitis in two experimental models in rats

1995 ◽  
Vol 17 (2) ◽  
pp. 147-154
Author(s):  
Issei Tachibana ◽  
Nobuaki Watanabe ◽  
Hisashi Shirohara ◽  
Toshiharu Akiyama ◽  
Shigekazu Nanano ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Exocrine Secretion ◽  
Experimental Models ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Exocrine

scholarly journals Developing Practical Therapeutic Strategies that Target Protein SUMOylation

2019 ◽  
Vol 20 (9) ◽  
pp. 960-969 ◽  
Author(s):  
Olivia F. Cox ◽  
Paul W. Huber
Keyword(s):  
Birth Defects ◽  
Inflammatory Disease ◽  
Intracellular Localization ◽  
Specific Protein ◽  
Therapeutic Strategies ◽  
Biological Processes ◽  
Post Translational Modification ◽  
Protein Activity ◽  
Multiple Components ◽  
Congenital Birth Defects

Post-translational modification by small ubiquitin-like modifier (SUMO) has emerged as a global mechanism for the control and integration of a wide variety of biological processes through the regulation of protein activity, stability and intracellular localization. As SUMOylation is examined in greater detail, it has become clear that the process is at the root of several pathologies including heart, endocrine, and inflammatory disease, and various types of cancer. Moreover, it is certain that perturbation of this process, either globally or of a specific protein, accounts for many instances of congenital birth defects. In order to be successful, practical strategies to ameliorate conditions due to disruptions in this post-translational modification will need to consider the multiple components of the SUMOylation machinery and the extraordinary number of proteins that undergo this modification.

scholarly journals Molecular Targets for the Treatment of Metastatic Colorectal Cancer

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2350
Author(s):  
Romain Cohen ◽  
Thomas Pudlarz ◽  
Jean-François Delattre ◽  
Raphaël Colle ◽  
Thierry André
Keyword(s):  
Colorectal Cancer ◽  
Molecular Targets ◽  
Predictive Biomarkers ◽  
Therapeutic Strategies ◽  
Her2 Amplification ◽  
Liquid Biopsies ◽  
Braf Mutations ◽  
Genetic Characteristics ◽  
New Developments ◽  
The Past

Over the past years, colorectal cancer (CRC) was subtyped according to its molecular and genetic characteristics, allowing the development of therapeutic strategies, based on predictive biomarkers. Biomarkers such as microsatellite instability (MSI), RAS and BRAF mutations, HER2 amplification or NTRK fusions represent major tools for personalized therapeutic strategies. Moreover, the routine implementation of molecular predictive tests provides new perspectives and challenges for the therapeutic management of CRC patients, such as liquid biopsies and the reintroduction of anti-EGFR monoclonal antibodies. In this review, we summarize the current landscape of targeted therapies for metastatic CRC patients, with a focus on new developments for EGFR blockade and emerging biomarkers (MSI, HER2, NTRK).

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