Adiponectin Synthesis, Secretion and Extravasation from Circulation to Interstitial Space

Physiology ◽  
2021 ◽  
Vol 36 (3) ◽  
pp. 134-149 ◽  
Author(s):  
Simone C. da Silva Rosa ◽  
Meilian Liu ◽  
Gary Sweeney

Adiponectin, an adipokine that circulates as multiple multimeric complexes at high levels in serum, has antidiabetic, anti-inflammatory, antiatherogenic, and cardioprotective properties. Understanding the mechanisms regulating adiponectin’s physiological effects is likely to provide critical insight into the development of adiponectin-based therapeutics to treat various metabolic-related diseases. In this review, we summarize our current understanding on adiponectin action in its various target tissues and in cellular models. We also focus on recent advances in two particular regulatory aspects; namely, the regulation of adiponectin gene expression, multimerization, and secretion, as well as extravasation of circulating adiponectin to the interstitial space and its degradation. Finally, we discuss some potential therapeutic approaches using adiponectin as a target and the current challenges facing adiponectin-based therapeutic interventions.

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.


2021 ◽  
Vol 14 (2) ◽  
pp. 96
Author(s):  
Susie L. Brown ◽  
Samantha Kendrick

Stretches of cytosine-rich DNA are capable of adopting a dynamic secondary structure, the i-motif. When within promoter regions, the i-motif has the potential to act as a molecular switch for controlling gene expression. However, i-motif structures in genomic areas of repetitive nucleotide sequences may play a role in facilitating or hindering expansion of these DNA elements. Despite research on the i-motif trailing behind the complementary G-quadruplex structure, recent discoveries including the identification of a specific i-motif antibody are pushing this field forward. This perspective reviews initial and current work characterizing the i-motif and providing insight into the biological function of this DNA structure, with a focus on how the i-motif can serve as a molecular target for developing new therapeutic approaches to modulate gene expression and extension of repetitive DNA.


Author(s):  
Dheeraj Pandey ◽  
Tiyas Pal ◽  
Abha Sharma ◽  
SJS Flora

Abstract:: Memory remains an obligatory regime of human brain and impaired memory causes serious obstacles in our everyday life. Alzheimer’s disease (AD) is one such neurodegenerative disease which is mostly affects elderly population, above the age of 60; marked by cognitive impairment of memory. Besides the known targets of AD against the several etiologies known till date, the zone of epigenetics has recently evolved as an ingenious field in AD. Epigenetic modifications do not affect DNA sequence but only long-term gene expression. Considering the multifactorial complex nature of AD, we herein discuss the various epigenetic targets which might give rise to potential therapeutic approaches. We reviewed the possible epigenetic targets for AD like HDAC, Sirtuins, glial cells, miRNA and epigenetic modifications like DNA methylation. A deeper insight into these target areas can surely evolve AD diagnosis and therapeutics.


2021 ◽  
Author(s):  
Rebecca A Rolfe ◽  
David Scanlon O'Callaghan ◽  
Paula Murphy

Fetal activity in utero is a normal part of pregnancy and reduced or absent movement can lead to long-term skeletal defects such as Fetal Akinesia Deformation Sequence (FADS), joint dysplasia and arthrogryposis. A variety of animal models with decreased or absent embryonic movements show a consistent set of developmental defects providing insight into the aetiology of congenital skeletal abnormalities. At developing joints defects include reduced joint interzones with frequent fusion of cartilaginous skeletal rudiments across the joint. At the spine defects include shortening and a spectrum of curvature deformations. An important question, with relevance to possible therapeutic interventions for human conditions, is the capacity for recovery with resumption of movement following short term immobilisation. Here we use the well-established chick model to compare the effects of sustained immobilisation from embryonic day (E) 4-10 to two different recovery scenarios: (i) natural recovery from E6 until E10 and (ii) the addition of hyperactive movement stimulation during the recovery period. We demonstrate partial recovery of movement and partial recovery of joint development under both recovery conditions, but no improvement in spine defects. The joints examined (elbow, hip and knee) showed better recovery in hindlimb than forelimb, with hyperactive mobility leading to greater recovery in the knee and hip. The hip joint showed the best recovery with improved rudiment separation, tissue organisation and commencement of cavitation. This work demonstrates that movement post paralysis can partially-recover specific aspects of joint development which could inform therapeutic approaches to ameliorate the effects of human fetal immobility.


2021 ◽  
pp. dmm.048913
Author(s):  
Rebecca A. Rolfe ◽  
David Scanlon O'Callaghan ◽  
Paula Murphy

Fetal activity in utero is a normal part of pregnancy and reduced or absent movement can lead to long-term skeletal defects such as Fetal Akinesia Deformation Sequence (FADS), joint dysplasia and arthrogryposis. A variety of animal models with decreased or absent embryonic movements show a consistent set of developmental defects providing insight into the aetiology of congenital skeletal abnormalities. At developing joints defects include reduced joint interzones with frequent fusion of cartilaginous skeletal rudiments across the joint. At the spine defects include shortening and a spectrum of curvature deformations. An important question, with relevance to possible therapeutic interventions for human conditions, is the capacity for recovery with resumption of movement following short term immobilisation. Here we use the well-established chick model to compare the effects of sustained immobilisation from embryonic day (E) 4-10 to two different recovery scenarios: (i) natural recovery from E6 until E10 and (ii) the addition of hyperactive movement stimulation during the recovery period. We demonstrate partial recovery of movement and partial recovery of joint development under both recovery conditions, but no improvement in spine defects. The joints examined (elbow, hip and knee) showed better recovery in hindlimb than forelimb, with hyperactive mobility leading to greater recovery in the knee and hip. The hip joint showed the best recovery with improved rudiment separation, tissue organisation and commencement of cavitation. This work demonstrates that movement post paralysis can partially-recover specific aspects of joint development which could inform therapeutic approaches to ameliorate the effects of human fetal immobility.


Author(s):  
Hannah Lee

This paper is the attempt to show how system theory could provide critical insight into the transdisciplinary field of library and information sciences (LIS). It begins with a discussion on the categorization of library and information sciences as an academic and professional field (or rather, the lack of evidence on the subject) and what is exactly meant by system theory, drawing upon the general system theory established by Ludwig von Bertalanffy. The main conversation of this paper focuses on the inadequacies of current meta-level discussions of LIS and the benefits of general system theory (particularly when considering the exponential rapidity in which information travels) with LIS.


2018 ◽  
Vol 1 (1) ◽  
pp. 18
Author(s):  
Kym Maclaren

“To consent to love or be loved,” said Merleau-Ponty, “is to consent also to influence someone else, to decide to a certain extent on behalf of the other.” This essay explicates that idea through a meditation on intimacy. I propose, first, that, on Merleau-Ponty’s account, we are always transgressing into each other’s experience, whether we are strangers or familiars; I call this “ontological intimacy.” Concrete experiences of intimacy are based upon this ontological intimacy, and can take place at two levels: (1) at-this-moment (such that we can experience intimacy even with strangers, by sharing a momentary but extra-ordinary mutual recognition) and (2) in shared interpersonal institutions, or habitual, enduring, and co-enacted visions of who we are, how to live, and what matters. Through particular examples of dynamics within these layers of intimacy (drawing upon work by Berne and by Russon), I claim that we are always, inevitably, imposing an “unfreedom” upon our intimate others. Freedom, then, can only develop from within and by virtue of this “unfreedom.” Thus, what distinguishes empowering or emancipating relationships from oppressive ones is not the removal of transgressive normative social forces; it is rather the particular character of those transgressive forces. Some transgressions upon others’ experience—some forms of “unfreedom”—will tend to promote freedom; others will tend to hinder it. This amounts to a call for promoting agency and freedom not only through critical analysis of public institutions, practices and discourses, but also through critical insight into and transformation of our most private and intimate relationships.


2020 ◽  
Vol 27 (20) ◽  
pp. 3330-3345
Author(s):  
Ana G. Rodríguez-Hernández ◽  
Rafael Vazquez-Duhalt ◽  
Alejandro Huerta-Saquero

Nanomaterials have become part of our daily lives, particularly nanoparticles contained in food, water, cosmetics, additives and textiles. Nanoparticles interact with organisms at the cellular level. The cell membrane is the first protective barrier against the potential toxic effect of nanoparticles. This first contact, including the interaction between the cell membranes -and associated proteins- and the nanoparticles is critically reviewed here. Nanoparticles, depending on their toxicity, can cause cellular physiology alterations, such as a disruption in cell signaling or changes in gene expression and they can trigger immune responses and even apoptosis. Additionally, the fundamental thermodynamics behind the nanoparticle-membrane and nanoparticle-proteins-membrane interactions are discussed. The analysis is intended to increase our insight into the mechanisms involved in these interactions. Finally, consequences are reviewed and discussed.


2020 ◽  
Vol 27 (7) ◽  
pp. 1052-1080 ◽  
Author(s):  
Evangelos Oikonomou ◽  
Gerasimos Siasos ◽  
Vasiliki Tsigkou ◽  
Evanthia Bletsa ◽  
Maria-Evi Panoilia ◽  
...  

Coronary artery disease is the leading cause of morbidity and mortality worldwide. The most common pathophysiologic substrate is atherosclerosis which is an inflammatory procedure that starts at childhood and develops throughout life. Endothelial dysfunction is associated with the initiation and progression of atherosclerosis and is characterized by the impaired production of nitric oxide. In general, endothelial dysfunction is linked to poor cardiovascular prognosis and different methods, both invasive and non-invasive, have been developed for its evaluation. Ultrasound evaluation of flow mediated dilatation of the branchial artery is the most commonly used method to assessed endothelial function while intracoronary administration of vasoactive agents may be also be used to test directly endothelial properties of the coronary vasculature. Endothelial dysfunction has also been the subject of therapeutic interventions. This review article summarizes the knowledge about evaluation of endothelial function in acute coronary syndromes and stable coronary artery disease and demonstrates the current therapeutic approaches against endothelial dysfunction.


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