Role of apolipoprotein E in renal damage protection

Bonomini, Francesca; Rodella, Luigi Fabrizio; Moghadasian, Mohammed H.; Lonati, Claudio; Coleman, Raymond; Rezzani, Rita

doi:10.1007/s00418-011-0815-1

Cited by 11 publications

(7 citation statements)

References 41 publications

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“…2002; Bonomini et al. 2011), and laboratory mutants show a number of physiological and morphological changes similar to kidney disease phenotypes (Bonomini et al. 2011).…”

Section: Resultsmentioning

confidence: 99%

Gene expression plasticity and desert adaptation in house mice*

2021

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Understanding how organisms adapt to new environments is a key problem in evolution, yet it remains unclear whether phenotypic plasticity generally facilitates or hinders this process. Here we studied evolved and plastic responses to water‐stress in lab‐born descendants of wild house mice (Mus musculus domesticus) collected from desert and non‐desert environments and measured gene expression and organismal phenotypes under control and water‐stressed conditions. After many generations in the lab, desert mice consumed significantly less water than mice from other localities, indicating that this difference has a genetic basis. Under water‐stress, desert mice maintained more weight than non‐desert mice, and exhibited differences in blood chemistry related to osmoregulatory function. Gene expression in the kidney revealed evolved differences between mice from different environments as well as plastic responses between hydrated and dehydrated mice. Desert mice showed reduced expression plasticity under water‐stress compared to non‐desert mice. Importantly, non‐desert mice under water‐stress generally showed shifts toward desert‐like expression, consistent with adaptive plasticity. Finally, we identify several co‐expression modules linked to phenotypes of interest. These findings provide evidence for local adaptation after a recent invasion and suggest that adaptive plasticity may have facilitated colonization of the desert environment.

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“…2002; Bonomini et al. 2011), and laboratory mutants show a number of physiological and morphological changes similar to kidney disease phenotypes (Bonomini et al. 2011).…”

Section: Resultsmentioning

confidence: 99%

Gene expression plasticity and desert adaptation in house mice*

2021

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“…It was also shown that mitochondrial ROS enhanced telomere-dependent senescence (Passos et al, 2007 ). Likewise, some authors showed the link between telomere length and metabolic disease suggesting increased cellular turnover and therefore accelerated cell aging (Bonomini et al, 2011 ; Kong et al, 2013 ). The increasing abdominal adiposity typical of the MetS is accompanied by accelerated telomere attrition (Révész et al, 2015 ).…”

Section: Pathophysiologymentioning

confidence: 98%

Metabolic Syndrome and Neuroprotection

et al. 2018

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Introduction: Over the years the prevalence of metabolic syndrome (MetS) has drastically increased in developing countries as a major byproduct of industrialization. Many factors, such as the consumption of high-calorie diets and a sedentary lifestyle, bolster the spread of this disorder. Undoubtedly, the massive and still increasing incidence of MetS places this epidemic as an important public health issue. Hereon we revisit another outlook of MetS beyond its classical association with cardiovascular disease (CVD) and Diabetes Mellitus Type 2 (DM2), for MetS also poses a risk factor for the nervous tissue and threatens neuronal function. First, we revise a few essential concepts of MetS pathophysiology. Second, we explore some neuroprotective approaches in MetS pertaining brain hypoxia. The articles chosen for this review range from the years 1989 until 2017; the selection criteria was based on those providing data and exploratory information on MetS as well as those that studied innovative therapeutic approaches.Pathophysiology: The characteristically impaired metabolic pathways of MetS lead to hyperglycemia, insulin resistance (IR), inflammation, and hypoxia, all closely associated with an overall pro-oxidative status. Oxidative stress is well-known to cause the wreckage of cellular structures and tissue architecture. Alteration of the redox homeostasis and oxidative stress alter the macromolecular array of DNA, lipids, and proteins, in turn disrupting the biochemical pathways necessary for normal cell function.Neuroprotection: Different neuroprotective strategies are discussed involving lifestyle changes, medication aimed to mitigate MetS cardinal symptoms, and treatments targeted toward reducing oxidative stress. It is well-known that the routine practice of physical exercise, aerobic activity in particular, and a complete and well-balanced nutrition are key factors to prevent MetS. Nevertheless, pharmacological control of MetS as a whole and pertaining hypertension, dyslipidemia, and endothelial injury contribute to neuronal health improvement.Conclusion: The development of MetS has risen as a risk factor for neurological disorders. The therapeutic strategies include multidisciplinary approaches directed to address different pathological pathways all in concert.

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“…According with this theory a study by Passos et al 2007 demonstrated that the senescent cells had higher ROS levels, dysfunctional mitochondria, more DNA double-strand breaks and shorter telomeres and it was shown that mitochondrial ROS enhanced telomeredependent senescence [137]. Recently, some authors showed the link between telomere length and metabolic disease suggesting increased cellular turnover and therefore accelerated cell aging [138,139]. …”

Section: Aging and Methabolic Syndromementioning

confidence: 99%

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

Bonomini¹,

Rodella²,

Rezzani³

2015

Aging and disease

491

322

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ABSTRACT:The prevalence of the metabolic syndrome, a cluster of cardiovascular risk factors associated with obesity and insulin resistance, is dramatically increasing in Western and developing countries. This disorder consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart diseases. One of the defects in metabolic syndrome and its associated diseases is excess of reactive oxygen species. Reactive oxygen species generated by mitochondria, or from other sites within or outside the cell, cause damage to mitochondrial components and initiate degradative processes. Such toxic reactions contribute significantly to the aging process. In this article we review current understandings of oxidative stress in metabolic syndrome related disease and its possible contribution to accelerated senescence.

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Role of apolipoprotein E in renal damage protection

Cited by 11 publications

References 41 publications

Gene expression plasticity and desert adaptation in house mice*

Gene expression plasticity and desert adaptation in house mice*

Metabolic Syndrome and Neuroprotection

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

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