Potential Role of Perilacunar Remodeling in the Progression of Osteoporosis and Implications on Age-Related Decline in Fracture Resistance of Bone

2021 ◽  
Author(s):  
Katharina Jähn-Rickert ◽  
Elizabeth A. Zimmermann
Keyword(s):  
Fracture Resistance ◽  
Potential Role ◽  
Age Related

scholarly journals Pleiotropic actions of estrogen: a mitochondrial matter

2013 ◽  
Vol 45 (3) ◽  
pp. 106-109 ◽  
Author(s):  
Michael C. Velarde
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cellular Response ◽  
Estrogen Replacement Therapy ◽  
Potential Role ◽  
Estrogen Replacement ◽  
Beneficial Effects ◽  
Age Related ◽  
Pleiotropic Action ◽  
Pleiotropic Actions

Estrogen provides many beneficial effects early in life by regulating normal tissue development and several physiological functions. While estrogen replacement therapy (ERT) in women was expected to reduce the health risks associated with the age-related decline in estrogen levels during menopause, ERT also resulted in increased progression to other types of diseases. Hence, distinguishing the signaling pathways that regulate the beneficial and detrimental effects of estrogen is important for developing interventions that selectively harness the hormone's beneficial effects, while minimizing its side effects. Estrogen can minimize mitochondrial dysfunction, which is thought to contribute to aging phenotypes. Decline in estrogen levels during menopause may lead to progressive mitochondrial dysfunction and may permanently alter cellular response, including that of estrogen (i.e., ERT). This review discusses the interplay between estrogen and mitochondrial function during the aging process and suggests a potential role of mitochondria in influencing the pleiotropic action of estrogen.

scholarly journals Epigenetics of aging and disease: a brief overview

2019 ◽  
Author(s):  
Christina Pagiatakis ◽  
Elettra Musolino ◽  
Rosalba Gornati ◽  
Giovanni Bernardini ◽  
Roberto Papait
Keyword(s):  
Gene Expression ◽  
Neurodegenerative Disorders ◽  
Potential Role ◽  
Molecular Level ◽  
Physiological Function ◽  
Regulate Gene Expression ◽  
Age Related ◽  
Genetic And Environmental Factors ◽  
Different Tissues

AbstractAging is an important risk factor for several human diseases such as cancer, cardiovascular disease and neurodegenerative disorders, resulting from a combination of genetic and environmental factors (e.g., diet, smoking, obesity and stress), which, at molecular level, cause changes in gene expression underlying the decline of physiological function. Epigenetics, which include mechanisms regulating gene expression independently of changes to DNA sequence, regulate gene expression by modulating the structure of chromatin or by regulating the binding of transcriptional machinery to DNA. Several studies showed that an impairment of epigenetic mechanisms promotes alteration of gene expression underlying several aging-related diseases. Alteration of these mechanisms is also linked with changes of gene expression that occurs during aging processes of different tissues. In this review, we will outline the potential role of epigenetics in the onset of two age-related pathologies, cancer and cardiovascular diseases.

Inflammatory Molecular Mediators and Pathways Involved in Vascular Aging and Stroke: A Comprehensive Review

2021 ◽  
Vol 28 ◽  
Author(s):  
Amro M. Soliman ◽  
Srijit Das ◽  
Pasuk Mahakkanukrauh
Keyword(s):  
Drug Targets ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Vascular Diseases ◽  
Vascular Aging ◽  
Inflammatory Conditions ◽  
Age Related ◽  
Cardiovascular Pathologies ◽  
Potential Drug Targets

: There is an increase in the incidence of cardiovascular diseases with aging and it is one of the leading causes of death worldwide. The main cardiovascular pathologies include atherosclerosis, stroke, myocardial infarction, hypertension and stroke. Chronic inflammation is one of the significant contributors to the age-related vascular diseases. Therefore, it is important to understand the molecular mechanisms of the persistent inflammatory conditions occurring in the blood vessels as well as the signaling pathways involved. Herein, we performed an extant search of literature involving PubMed, ISI, WoS and Scopus databases for retrieving all relevant articles with the most recent findings illustrating the potential role of various inflammatory mediators along with their proposed activated pathways in the pathogenesis and progression of vascular aging. We also highlight the major pathways contributing to age-related vascular disorders. The outlined molecular mechanisms, pathways and mediators of vascular aging represent potential drug targets that can be utilized to inhibit and/or slow the pathogenesis and progression of vascular aging.

Neuromuscular contributions to the age-related reduction in muscle power: Mechanisms and potential role of high velocity power training

2017 ◽  
Vol 35 ◽  
pp. 147-154 ◽  
Author(s):  
Neal B. McKinnon ◽  
Denise M. Connelly ◽  
Charles L. Rice ◽  
Susan W. Hunter ◽  
Timothy J. Doherty
Keyword(s):  
High Velocity ◽  
Potential Role ◽  
Muscle Power ◽  
Power Training ◽  
Age Related

Fracture of SnBi/Ni(P) interfaces

2005 ◽  
Vol 20 (4) ◽  
pp. 818-826 ◽  
Author(s):  
P.L. Liu ◽  
J.K. Shang
Keyword(s):  
Fracture Mechanism ◽  
Fracture Resistance ◽  
Potential Role ◽  
Substrate Interface ◽  
Interfacial Segregation ◽  
The Difference ◽  
Cu Interconnect ◽  
Electroless Ni ◽  
Bi Segregation

Fracture resistance of the interface between electroless Ni(P) and the eutectic SnBi solder alloy was examined in the as-reflowed and aged conditions, to investigate the potential role of Ni in inhibiting interfacial segregation of Bi in SnBi–Cu interconnect. In the as-reflowed condition, the fracture resistance of the SnBi/Ni(P) interface was about the same as that of the SnBi/Cu interface. Upon aging at 120 °C for 7 days the fracture resistance of the SnBi/Ni(P) interface was much higher than that of the SnBi/Cu interface. Such a difference was shown to result from the difference in fracture mechanism as the crack remained along the solder–intermetallic interface in the aged SnBi–Ni interconnect but propagated along the intermetallic–substrate interface in the aged SnBi–Cu interconnect. While fracture of the intermetallic–substrate interface in SnBi–Cu interconnect was due to Bi segregation onto that interface, no Bi was detected at the intermetallic-substrate interface in SnBi–Ni interconnects, implying that Ni(P) was effective in inhibiting the interfacial segregation of Bi.

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