China
Africa
Explore chapters and articles related to this topic
Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Hashim Islam, Jacob T. Bonafiglia, Cesare Granata, Brendon J. Gurd
Similar to PPARβ, the oestrogen-related receptor (ERR) family of nuclear receptors are known regulators of oxidative metabolism, and their transcriptional activity is dependent on their interactions with various co-regulators (e.g., PGC-1a) (62). However, transgenic rodent studies suggest that oxidative remodelling of skeletal muscle by the gamma-isoform of this family (ERRg) may also occur independently from PGC-1a (25). Overexpression of ERRg in murine skeletal muscle increases mitochondrial content, oxidative enzyme activities, and exercise capacity (62). Most compellingly, ERRg overexpression in murine skeletal muscle devoid of both PGC-1 isoforms (PGC-1a/β) significantly improves defects in mitochondrial content and respiratory function associated with the loss of PGC-1a/β both basally and in response to exercise training (25). These findings implicate ERRg as an additional player in the transcriptional control of mitochondrial biogenesis beyond its established role as a downstream binding partner of PGC-1a.
Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The mean uBPA concentration in our study was 3.65 ng/mL with an assumption of an average 24-hour urine volume for adults of 1600 mL, a 100% excretion rate, and a total blood volume of 6 L, which would give an estimated BPA blood concentration in the nanograms per milliliter range. BPA shows relatively weak estrogenic agonist activities against both human estrogen receptor-α and receptor-β subtypes (ERα, ERβ) that control many estrogen-mediated activities. The half-maximal inhibitory concentration for receptor binding of BPA to human ERα and ERβ is in the low micromolar range when calculated in vitro and, if extrapolated directly to the in vivo situation (without considering competitive binding to serum-binding proteins, for instance), this would imply low ER occupancy rates in blood and potential target tissues. However, BPA binds to other estrogen-related receptors with high affinity, including the estrogen-related receptor-γ (ERRγ), for which optimal receptor binding is in the nanomolar range.277 A recent study has reported positive associations between increased BPS exposure and in vivo estrogenic gene expression in adults, including ERβ and the estrogen-related receptor α (ERRα).278 ERRα is an orphan nuclear receptor involved in estrogenic signaling and energy homeostatis that is coordinately regulated with ERRγ. It is relevant to note that expression of ERRα is highest in tissues that preferentially use fatty acids as energy sources, including adipose tissue, skeletal muscle, and heart.
Vulvar lichen sclerosus
Published in Miranda A. Farage, Howard I. Maibach, The Vulva, 2017
Jill M. Krapf, Andrew T. Goldstein
Estrogen and androgen deficiency has been explored as a potential cause of LS, related to a defect in the enzyme 5a-reductase (22). This may explain the lack of efficacy of hormonal therapies in LS (2). In an analysis of 110 samples, estrogen-related receptor-a (ERR-a), a regulator of cell energy metabolism and inflammatory processes, was found to be reduced in almost 80% of patients with childhood-onset LS and 51% of patients with adult-onset LS. Absence or a substantial reduction in ERR-a was found in all 50 samples of vulvar squamous cell carcinoma (SCC), indicating that estrogen receptor expression may play a role in the pathogenesis of LS and related vulvar SCC (23).
Kidney and lipids: novel potential therapeutic targets for dyslipidemia in kidney disease?
Published in Expert Opinion on Therapeutic Targets, 2022
Konrad Zuzda, Wiktoria Grycuk, Jacek Małyszko, Jolanta Małyszko
In another model of diabetic DBA/2 J and db/db mice, Wang et al. [178] reported that the nuclear hormone receptor farnesoid X receptor (FXR) and G protein–coupled receptor TGR5 have renoprotective roles in diabetes- and obesity-related kidney diseases. Administration of the dual FXR/TGR5 agonist INT-767 improved proteinuria and prevented podocyte injury, mesangial expansion, and tubulointerstitial fibrosis. This agent affects multiple pathways, including stimulation of a signaling cascade involving AMP-activated protein kinase, sirtuin 1, PGC-1α (peroxisome proliferator-activated receptor-gamma coactivator), sirtuin 3, estrogen-related receptor-α, and Nrf-1, inhibition of endoplasmic reticulum stress, and inhibition of enhanced renal fatty acid and cholesterol metabolism. In addition, in mice with diet-induced obesity, a dual FXR/TGR5 agonist prevents mitochondrial dysfunction, oxidative stress, and kidney fibrosis. The authors suggested that INT-767 could be a promising agent for the treatment of renal complications in diabetes and obesity. As angiotensin II exacerbates mitochondrial reactive oxygen species synthesis and mitochondrial fragmentation in podocytes, both in vivo and in vitro, Zhu et al. [179] recently showed that mitoquinone, a mitochondria-targeted antioxidant, can reverse injury caused by angiotensin II.
Low bone mass is associated with carotid calcification plaque in Chinese postmenopausal women: the Chongqing osteoporosis study
Published in Climacteric, 2020
D. Liu, L. Chen, S. Dong, H. Yang, L. Li, J. Liu, H. Zhou, R. Zhou
Vascular calcification is now considered to be an active process with common characteristics with bone remodeling48–51. The study has suggested that heparanase may play an important role in vascular calcification, which may be related to the enhancement of mineralization and osteogenic differentiation of vascular smooth muscle cells7. Dynamic protein-related protein 1 (DRP1) is a key regulator of mitochondrial division. The data demonstrated a new function of DRP1 in regulating cardiovascular calcification, and supported a role of mitochondrial dynamics in regulating oxidative stress-mediated arterial calcium accrual and bone loss52. Vascular calcification which refers to ectopic mineralization in vascular cells is associated with atherosclerosis53. The present results indicated that estrogen-related receptor (ERR) γ played a key role in vascular calcification by upregulating the BMP2 signaling pathway. ERRγ promoted dedifferentiation of vascular smooth muscle cells to an osteogenic phenotype during the vascular calcification process. Runt-related transcription factor 2 (Runx2) is a key osteogenic transcription factor; the present studies have demonstrated that Runx2 is related to calcification of vascular smooth muscle cells54. The study has determined a new causative effect of vascular smooth muscle cell-specific phosphatase on vascular calcification, and has demonstrated that FOXO1/3 (forkhead box O) plays a crucial role in Runx2 ubiquitination and vascular smooth muscle cell calcification.
miRNA-378a as a key regulator of cardiovascular health following engineered nanomaterial inhalation exposure
Published in Nanotoxicology, 2019
Quincy A. Hathaway, Andrya J. Durr, Danielle L. Shepherd, Mark V. Pinti, Ashley N. Brandebura, Cody E. Nichols, Amina Kunovac, William T. Goldsmith, Sherri A. Friend, Alaeddin B. Abukabda, Garrett K. Fink, Timothy R. Nurkiewicz, John M. Hollander
Opa1, a direct mediator with Mfn1 of inducing mitochondrial fusion, was shown to be significantly increased in the Het and KO groups following inhalation exposure; likewise, expression of the fatty acid metabolism protein Pparα was also increased (Figure S6(B)). The knockdown/knockout of miRNA-378a-5p, which acts as a negative regulator of estrogen-related receptor gamma (EERγ) and GA-binding protein alpha chain (GABPA), could promote the expression of PGC-1β and subsequently interact with Pparα (Eichner et al. 2010). In the KO animal, PGC-1β is found to be significantly increased compared to the WT group, following inhalation exposure (Figure S6(C)). Following maternal nano-TiO2 exposure, PGC-1β displayed increased histone 3 lysine 4 tri-methylation (H3K4me3) association at its promoter region, suggesting an increased expression of both the gene and miRNA-378a through epigenetic mechanisms (Figure S6(D)) (Stapleton et al. 2018). Suppressing miRNA-378a during inhalation exposure could diminish cardiac dysfunction by offering cardioprotection through pathways including transcription, bioenergetics, fatty acid metabolism, and mitochondrial fusion (Figure 6(A,B)).