scholarly journals An Update on Inflamm-Aging: Mechanisms, Prevention, and Treatment

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Shijin Xia ◽  
Xinyan Zhang ◽  
Songbai Zheng ◽  
Ramin Khanabdali ◽  
Bill Kalionis ◽  
...  

Inflamm-aging is a challenging and promising new branch of aging-related research fields that includes areas such as immunosenescence. Increasing evidence indicates that inflamm-aging is intensively associated with many aging diseases, such as Alzheimer’s disease, atherosclerosis, heart disease, type II diabetes, and cancer. Mounting studies have focused on the role of inflamm-aging in disease progression and many advances have been made in the last decade. However, the underlying mechanisms by which inflamm-aging affects pathological changes and disease development are still unclear. Here, we review studies of inflamm-aging that explore the concept, pathological features, mechanisms, intervention, and the therapeutic strategies of inflamm-aging in disease progression.

2018 ◽  
Vol 45 (3) ◽  
pp. 1023-1033 ◽  
Author(s):  
Weina Cao ◽  
Yatao Xu ◽  
Dan Luo ◽  
Muhammad Saeed ◽  
Chao Sun

Background/Aims: Impaired adipogenesis may be the underlying cause in the development of obesity and type II diabetes. Mechanistically, the family of Homeobox transcription factors is implicated in the regulation of adipocyte fate. Hoxa5 is highly expressed in adipocytes, and its mRNA expression is decreased during differentiation. However, the function of Hoxa5 in adipose tissue has been poorly understood. The aim of this study is to unveil the role of Hoxa5 on adipocyte differentiation and its underlying mechanisms. Methods: Quantitative real-time PCR (qPCR) and western blot were performed to determine Hoxa5 expression in primary adipocytes and in adipose tissues from mice. Lipid accumulation was evaluated by bodipy staining. Dual luciferase assay was applied to explore the transcription factor of Hoxa5 and the transcriptional target gene modulated by Hoxa5. All measurements were performed at least for three times at least. Results: A significant reduction of Hoxa5 expression was observed in adipose tissue of High Fat Diet (HFD) induced obesity mice. We determined Hoxa5 increased adipocytes differentiation and mitochondrial biogenesis in adipocytes in vitro. CEBPβ was determined a transcription factor of Hoxa5 and inhibited methylation level of Hoxa5 by combining on the promoter of Hoxa5. Importantly, we found Fabp4, a known positive regulator of adipocytes differentiation, was transcriptional activation by Hoxa5. In addition, Hoxa5 promotes adipocytes differentiation by inhibiting PKA/HSL pathway. Conclusion: Our study demonstrated the promoting role of Hoxa5 in adipocytes differentiation and therefore bringing a new therapeutic mean to the treatment of obesity and type II diabetes.


Diabetes ◽  
1987 ◽  
Vol 36 (11) ◽  
pp. 1341-1350 ◽  
Author(s):  
J. P. Felber ◽  
E. Ferrannini ◽  
A. Golay ◽  
H. U. Meyer ◽  
D. Theibaud ◽  
...  

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Maria C. Barbosa-Silva ◽  
Maiara N. Lima ◽  
Denise Battaglini ◽  
Chiara Robba ◽  
Paolo Pelosi ◽  
...  

AbstractInfectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood–brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation. Graphic abstract


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Britta Larsen ◽  
Matthew Allison ◽  
Eugene Kang ◽  
Sarah Saad ◽  
Gail A Laughlin ◽  
...  

Background: Excess abdominal adipose tissue has been identified as an important factor in the development of type II diabetes. Lean muscle tissue also plays an important role in glucose regulation, yet research on the role of muscle in diabetes etiology is limited. Abdominal muscle mass could be particularly relevant for normal weight diabetics, for whom excessive abdominal adipose tissue may play less of a role. Objective: To explore the association between muscle-to-abdominal cavity area ratio and prevalent diabetes in older community-dwelling women in the Rancho Bernardo Study, UCSD Filipino Women’s Health Study, and the Health Assessment Study of African-American Women. Methods: Participants were 421 women (40% Caucasian, 28% Filipina, 32% African American) with a mean age of 64 (6.9) years. Abdominal muscle and fat areas were measured using computed tomography (CT) scans, and were used to compute a muscle-to-abdominal cavity area ratio (MACR). Based on body mass index (BMI), participants were classified as normal weight (18-24.9 kg/m2), overweight (25-29.9), or obese (30+). Prevalent diabetes was defined as self-report of physician diagnosis, anti-diabetes medication use, fasting morning glucose ≥ 126 mg/dL or 2 hour glucose ≥ 200mg/dL. MACR was modeled per standard deviation (SD) and logistic regression was used to examine the association with diabetes while adjusting for relevant covariates. Results: Prevalent diabetes was seen in 12.8% of the sample (54 of 421). In age and race/ethnicity adjusted models, each SD increase in MACR was associated with significant reduced odds of diabetes (OR = 0.62, CI: 0.43-0.89, p = 0.01), which remained significant after further adjustment for BMI category, smoking, physical activity, hypertension, anti-hypertensive drugs, and estrogen use (OR = 0.64, CI: 0.41-0.98, p = .041). The association was modestly attenuated after further adjusting for visceral fat area (OR = 0.70, CI: 0.44-1.10, p = 0.12). Normal weight women with diabetes had significantly less total muscle (p = 0.045) and smaller MACR’s (p = 0.001) than those without diabetes, while this was not seen for overweight or obese women with diabetes. Stratified by BMI category, MACR was significantly associated with lower odds of diabetes for normal weight women across all three models (fully adjusted OR = 0.37, CI: 0.15-0.90, p =.03), yet was not associated with diabetes in any models for women who were overweight or obese (all p > 0.50). Interactions of MACR with race/ethnicity were not significant. Conclusions: Muscle-to-abdominal cavity ratio is associated with reduced likelihood of type II diabetes in women. This association differs by BMI category, with muscle showing the greatest protection in normal weight women, and no effect in overweight or obese women. This highlights the potential role of low muscle mass as a risk factor for diabetes, particularly in women who may appear to be at low risk.


2021 ◽  
Vol 12 ◽  
Author(s):  
Sugyeong Jo ◽  
Sungsoon Fang

Increased incidence of type I and type II diabetes has been prevailed worldwide. Though the pathogenesis of molecular mechanisms remains still unclear, there are solid evidence that disturbed immune homeostasis leads to pancreatic β cell failure. Currently, autoimmunity and uncontrolled inflammatory signaling pathways have been considered the major factors in the pathogenesis of diabetes. Many components of immune system have been reported to implicate pancreatic β cell failure, including helper T cells, cytotoxic T cells, regulatory T cells and gut microbiota. Immune modulation of those components using small molecules and antibodies, and fecal microbiota transplantation are undergoing in many clinical trials for the treatment of type I and type II diabetes. In this review we will discuss the basis of molecular pathogenesis focusing on the disturbed immune homeostasis in type I and type II diabetes, leading to pancreatic β cell destruction. Finally, we will introduce current therapeutic strategies and clinical trials by modulation of immune system for the treatment of type I and type II diabetes patients.


2021 ◽  
Vol 68 (1) ◽  
pp. 77-86
Author(s):  
Iuliana Pantelimon ◽  
◽  
Laurentia Nicoleta Gales ◽  
Maria Daniela Tanasescu ◽  
Irina Nita ◽  
...  

Introduction. Breast cancer is the leading cause of cancer death in Romania. In the context in which the treatments available for this pathology have increased curability, the identification of negative prognostic factors involved in the evolution of this disease seems essential to improve the overall survival as well as the time to disease progression. Aim. The aim of this study is to identify the role of prognostic factors such as ki67 proliferation index, the presence of tumour estrogen receptors, HER2 overexpression, the presence of secondary determinations at diagnosis, the association of obesity and type II diabetes. Methods. 50 patients diagnosed with breast cancer treated in the Elias University Emergency Hospital Bucharest were retrospectively followed, for which the progression was documented at the time of elaboration of this study. Thus, a database was developed in which data were entered on age, body mass index, immunohistochemical characteristics of breast tumours, the presence/absence of metastases at diagnosis and the association of type II diabetes. Statistical calculations were performed to highlight a possible correlation between obesity (quantified by measuring body mass index) and tumour aggressiveness (quantified by ki67 proliferation index) as well as statistical evaluation of potential prognostic factors that would influence time, until the disease progresses. Results. Within this group, no correlation could be established between the presence of an increased body mass index and the value of the ki67 proliferation index (p = 0.38). The mean value of the body mass index for this group of unselected patients was 28.76 ± 4.81 (DS) most patients are therefore overweight or obese. The factors involved in the evolution of breast cancer that influenced the early progression of the disease were: the proliferation index ki67 (p <0.05), the presence of metastases at diagnosis (p < 0.0001) and the association of type II diabetes (p = 0.0085). The value of the body mass index did not influence the time to disease progression according to statistical calculations in this group probably due to the small number of normal weight patients included (p = 0.34).


Author(s):  
Oscar Herreras ◽  
Julia Makarova ◽  
José Manuel Ibarz

Neurons send trains of action potentials to communicate each other. Different messages are issued according to varying inputs, but they can also mix them up in a multiplexed language transmitted through a single cable, the axon. This remarkable property arises from the capability of dendritic domains to work semi autonomously and even decide output. We review the underlying mechanisms and theoretical implications of the role of voltage-dependent dendritic currents on the forward transmission of synaptic inputs, with special emphasis in the initiation, integration and forward conduction of dendritic spikes. When these spikes reach the axon, output decision was made in one of many parallel dendritic substations. When failed, they still serve as an internal language to transfer information between dendritic domains. This notion brakes with the classic view of neurons as the elementary units of the brain and attributes them computational/storage capabilities earlier billed to complex brain circuits.


2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Joshua A. David ◽  
William J. Rifkin ◽  
Piul S. Rabbani ◽  
Daniel J. Ceradini

Despite improvements in awareness and treatment of type II diabetes mellitus (TIIDM), this disease remains a major source of morbidity and mortality worldwide, and prevalence continues to rise. Oxidative damage caused by free radicals has long been known to contribute to the pathogenesis and progression of TIIDM and its complications. Only recently, however, has the role of the Nrf2/Keap1/ARE master antioxidant pathway in diabetic dysfunction begun to be elucidated. There is accumulating evidence that this pathway is implicated in diabetic damage to the pancreas, heart, and skin, among other cell types and tissues. Animal studies and clinical trials have shown promising results suggesting that activation of this pathway can delay or reverse some of these impairments in TIIDM. In this review, we outline the role of oxidative damage and the Nrf2/Keap1/ARE pathway in TIIDM, focusing on current and future efforts to utilize this relationship as a therapeutic target for prevention, prognosis, and treatment of TIID.


2016 ◽  
Vol 25 ◽  
pp. 104-112 ◽  
Author(s):  
Vinod Kumar ◽  
Aarti Jagannathan ◽  
Mariamma Philip ◽  
Arun Thulasi ◽  
Praveen Angadi ◽  
...  

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