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Oroxylin A ameliorates AKI-to-CKD transition through maintaining PPAR α-BNIP3 signaling-mediated mitochondrial homeostasis
Conclusion: Our findings revealed that OA ameliorates AKI-to-CKD transition by maintaining mitochondrial homeostasis through inducing PPARα-BNIP3 signaling pathway, indicating that OA may serve as a candidate therapeutic strategy for alleviating AKI and CKD.
Source: Frontiers in Pharmacology - August 23, 2022 Category: Drugs & Pharmacology Source Type: research

Loss and gain of function of Grp75 or mitofusin 2 distinctly alter cholesterol metabolism, but all promote triglyceride accumulation in hepatocytes
In conclusion, Grp75 or Mfn2 silencing and overexpression in Huh7 cells contribute to altering MAM integrity and cholesterol storage in opposite directions, but all promote triglyceride accumulation through distinct cellular pathways. This study also highlights that besides Mfn2, Grp75 could play a central role in hepatic lipid and cholesterol metabolism in obesity and NAFLD.PMID:34419589 | DOI:10.1016/j.bbalip.2021.159030
Source: Mol Biol Cell - August 22, 2021 Category: Molecular Biology Authors: Arthur Bassot Carina Prip Buus Ana ïs Alves Olivier Berdeaux Johan Perrier V éronique Lenoir Jingwei Ji-Cao Marie-Agn ès Berger Emmanuelle Loizon Stephanie Cabaret Baptiste Panthu Jennifer Rieusset B éatrice Morio Source Type: research

Effect of Forkhead Box O1 in Renal Tubular Epithelial Cells on Endotoxin-Induced Acute Kidney Injury.
In conclusion, downregulation of FOXO1 in RTECs mediated endotoxin-induced AKI and mitochondrial damage. Overexpression of FOXO1 could improve renal injury and mitochondrial dysfunction, and this effect occurred at least in part as a result of PGC1-α signaling. FOXO1 might be a potential target for the prevention and treatment of endotoxin-induced AKI. PMID: 33356954 [PubMed - as supplied by publisher]
Source: Am J Physiol Renal P... - December 28, 2020 Category: Urology & Nephrology Authors: Zhang M, Dong W, Li Z, Xiao Z, Xie Z, Ye Z, Liu S, Li R, Chen Y, Zhang L, Wang M, Liang H, Baihetiyaer R, Apaer R, Dong Z, Liang X Tags: Am J Physiol Renal Physiol Source Type: research

Brain Dicer1 Is Down-Regulated in a Mouse Model of Alzheimer ’s Disease Via Aβ42-Induced Repression of Nuclear Factor Erythroid 2-Related Factor 2
This study may open new avenues for investigating potential pathognomonics and pathogenesis in AD.
Source: Molecular Neurobiology - September 24, 2020 Category: Neurology Source Type: research

Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Resveratrol Promotes Diabetic Wound Healing via SIRT1-FOXO1-c-Myc Signaling Pathway-Mediated Angiogenesis
Conclusion: Our findings indicate that the positive role of RES in diabetic wound healing via its SIRT1-dependent endothelial protection and pro-angiogenic effects involves the inhibition of FOXO1 and the de-repression of c-Myc expression. Introduction Diabetes mellitus is a metabolic disease with an increasing incidence worldwide (Zimmet et al., 2014). The disease often leads to the development of serious complications such as microangiopathy, mainly including retinopathy, nephropathy, neuropathy, and diabetic non-healing skin ulcers (Zheng et al., 2018). Diabetic non-healing skin ulcers such as foot ulcers are ca...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

BOLA3 Deficiency Controls Endothelial Metabolism and Glycine Homeostasis in Pulmonary Hypertension.
CONCLUSIONS: BOLA3 acts as a crucial lynchpin connecting Fe-S-dependent oxidative respiration and glycine homeostasis with endothelial metabolic re-programming critical to PH pathogenesis. These results provide a molecular explanation for the clinical associations linking PH with hyperglycinemic syndromes and mitochondrial disorders. These findings also identify novel metabolic targets, including those involved in epigenetics, iron-sulfur biogenesis, and glycine biology, for diagnostic and therapeutic development. PMID: 30759996 [PubMed - as supplied by publisher]
Source: Circulation - February 14, 2019 Category: Cardiology Authors: Yu Q, Tai YY, Tang Y, Zhao J, Negi V, Culley MK, Pilli J, Sun W, Brugger K, Mayr J, Saggar R, Saggar R, Wallace WD, Ross DJ, Waxman AB, Wendell SG, Mullett SJ, Sembrat J, Rojas M, Khan OF, Dahlman JE, Sugahara M, Kagiyama N, Satoh T, Zhang M, Feng N, Gorc Tags: Circulation Source Type: research

Estrogen signaling increases nuclear receptor subfamily 4 group A member 1 expression and energy production in skeletal muscle cells.
Authors: Nagai S, Ikeda K, Horie-Inoue K, Takeda S, Inoue S Abstract Estrogen deficiency has been known to associate with musculoskeletal diseases in women, based on the clinical observations of frequent susceptibility to osteoporosis and sarcopenia among postmenopausal women. In skeletal muscles, estrogen has been assumed to play physiological roles in maintaining muscle mass and strength, although its precise molecular mechanism remains to be elucidated. We have previously shown that estrogen regulates energy metabolism through the downregulation of mitochondrial uncoupling protein 3 (UCP3) in skeletal muscles, w...
Source: Endocrine Journal - October 20, 2018 Category: Endocrinology Tags: Endocr J Source Type: research

Thyroid hormone (T3) stimulates brown adipose tissue activation via mitochondrial biogenesis and MTOR-mediated mitophagy.
Abstract The thyroid hormone triiodothyronine (T3) activates thermogenesis by uncoupling electron transport from ATP synthesis in brown adipose tissue (BAT) mitochondria. Although T3 can induce thermogenesis by sympathetic innervation, little is known about its cell autonomous effects on BAT mitochondria. We thus examined effects of T3 on mitochondrial activity, autophagy, and metabolism in primary brown adipocytes and BAT and found that T3 increased fatty acid oxidation and mitochondrial respiration as well as autophagic flux, mitophagy, and mitochondrial biogenesis. Interestingly, there was no significant induct...
Source: Autophagy - September 13, 2018 Category: Cytology Authors: Yau WW, Singh BK, Lesmana R, Zhou J, Sinha RA, Wong KA, Wu Y, Bay BH, Sugii S, Sun L, Yen PM Tags: Autophagy Source Type: research