Estrogenic control of mitochondrial function

Klinge, Carolyn M.

doi:10.1016/j.redox.2020.101435

Cited by 173 publications

(135 citation statements)

References 201 publications

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“…First, we did not include a histochemistry analysis of mitochondrial respiratory chain complexes and mitochondrial ultrastructure examination in heart tissues that can provide important information to prove the relationship between mitochondrial dysfunction and aging. Second, since female hormones (e.g., estrogen) regulate mitochondrial function [31], we used only male rats, including very young (1 months), young (4 months), middle-aged (10 months), and old (20 months) rats as animal models in this study.…”

Section: Discussionmentioning

confidence: 99%

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts

Choi

Cho

et al. 2020

Life

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Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart. However, the mechanism of mitochondria-mediated apoptosis in aged hearts remains poorly understood. Here, we used male Fischer 344 rats of various ages, representing very young (1 month), young (4 months), middle-aged (12 months), and old (20 months) rats, to determine whether mitochondria-mediated apoptotic signals and apoptosis in the left ventricle of the heart are altered notably with aging. As the rats aged, the extramyocyte space and myocyte cross-sectional area in their left ventricle muscle increased, while the number of myocytes decreased. Additionally, mitochondrion-mediated apoptotic signals and apoptosis increased remarkably during aging. Therefore, our results demonstrate that aging promotes remarkable morphological changes and increases the degree of mitochondrion-mediated apoptosis in the left ventricle of rat hearts.

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Section: Discussionmentioning

confidence: 99%

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts

Choi

Cho

et al. 2020

Life

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“…This is partly ascribed to the effect of sex hormones on the immune system and their interaction with environmental and genetic factors (Alpizar-Rodriguez et al, 2017). Estrogenic control of mitochondrial function and glycolysis metabolism has been studied (Cai et al, 2013;Klinge, 2020), however what are the sexbased differences in RA cell immunometabolism is still unknown and needs further investigation.…”

Section: Conclusion and Further Perspectivesmentioning

confidence: 99%

Metabolic Checkpoints in Rheumatoid Arthritis

et al. 2020

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Several studies have highlighted the interplay between metabolism, immunity and inflammation. Both tissue resident and infiltrating immune cells play a major role in the inflammatory process of rheumatoid arthritis (RA) via the production of cytokines, adipocytokines and metabolic intermediates. These functions are metabolically demanding and require the most efficient use of bioenergetic pathways. The synovial membrane is the primary site of inflammation in RA and exhibits distinctive histological patterns characterized by different metabolism, prognosis and response to treatment. In the RA synovium, the high energy demand by stromal and infiltrating immune cells, causes the accumulation of metabolites, and adipo-cytokines, which carry out signaling functions, as well as activating transcription factors which act as metabolic sensors. These events drive immune and joint-resident cells to acquire pro-inflammatory effector functions which in turn perpetuate chronic inflammation. Whether metabolic changes are a consequence of the disease or one of the causes of RA pathogenesis is still under investigation. This review covers our current knowledge of cell metabolism in RA. Understanding the intricate interactions between metabolic pathways and the inflammatory and immune responses will provide more awareness of the mechanisms underlying RA pathogenesis and will identify novel therapeutic options to treat this disease.

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“…Glucocorticoids also affect the fate of the main gluconeogenic precursors, amino acids, and altering the excretion of N [ 238 , 239 ]. Testosterone pairs with insulin as a main anabolic hormone [ 240 ], but glucocorticoids tend to limit testosterone production and availability [ 241 ], also affecting the availability of estrogen [ 242 ], which plays a critical function favoring the oxidation of 2C (i.e., saving 3C) in females [ 243 ] via direct intervention in mitochondrial function [ 244 , 245 ], and also preventing liver steatosis [ 246 ]. An estrogen-derivative has been found to down-modulate the adjustment of the ponderostat, i.e., the oxidation/mobilization of lipids from adipose tissue [ 247 , 248 ], by decreasing food intake and maintaining thermogenesis [ 249 ].…”

Section: Normalization and Regulation Under Excess (If Any)mentioning

confidence: 99%

“…In the liver, glucocorticoids increase glucose output [ 237 ] and favor lipogenesis [ 259 ] and TAG deposition in most tissues [ 260 ]; testosterone induces the accrual of protein [ 261 , 262 ] and stabilizes the maintenance of glycaemia [ 252 ]. Estrogens favor 2C oxidation [ 263 ], increase oxidative metabolism in mitochondria [ 245 ], and limit lipogenesis and TAG deposition [ 264 ]. The role of these steroid hormones on the direct modulation of glucose is less clear, despite the large number of agents and effects uncovered.…”

Section: Normalization and Regulation Under Excess (If Any)mentioning

confidence: 99%

Dietary Energy Partition: The Central Role of Glucose

Remesar

Alemany

2020

IJMS

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Humans have developed effective survival mechanisms under conditions of nutrient (and energy) scarcity. Nevertheless, today, most humans face a quite different situation: excess of nutrients, especially those high in amino-nitrogen and energy (largely fat). The lack of mechanisms to prevent energy overload and the effective persistence of the mechanisms hoarding key nutrients such as amino acids has resulted in deep disorders of substrate handling. There is too often a massive untreatable accumulation of body fat in the presence of severe metabolic disorders of energy utilization and disposal, which become chronic and go much beyond the most obvious problems: diabetes, circulatory, renal and nervous disorders included loosely within the metabolic syndrome. We lack basic knowledge on diet nutrient dynamics at the tissue-cell metabolism level, and this adds to widely used medical procedures lacking sufficient scientific support, with limited or nil success. In the present longitudinal analysis of the fate of dietary nutrients, we have focused on glucose as an example of a largely unknown entity. Even most studies on hyper-energetic diets or their later consequences tend to ignore the critical role of carbohydrate (and nitrogen disposal) as (probably) the two main factors affecting the substrate partition and metabolism.

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Estrogenic control of mitochondrial function

Cited by 173 publications

References 201 publications

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts

Metabolic Checkpoints in Rheumatoid Arthritis

Dietary Energy Partition: The Central Role of Glucose

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