1,244 results match your criteria bnip3

The role and mechanism of PKM2 in the development of LPS-induced acute kidney injury.

Histol Histopathol 2021 May 12:18343. Epub 2021 May 12.

Shanghai General Hospital of Nanjing Medical University, Shanghai, China.

A previous study suggested that pyruvate kinase M2 (PKM2) plays a vital role of metabolic reprogramming in the regulation of the innate inflammatory response, while PKM2 is a sensitive biomarker for nephrotoxicity. In this study, we investigated the role and mechanism of PKM2 in development of LPS-induced acute kidney injury. The AKI model of mice was established using LPS. Read More

View Article and Full-Text PDF

Significances of viable synergistic autophagy-associated cathepsin B and cathepsin D (CTSB/CTSD) as potential biomarkers for sudden cardiac death.

BMC Cardiovasc Disord 2021 May 8;21(1):233. Epub 2021 May 8.

School of Forensic Medicine, Guizhou Medical University, 4 Beijing Road, Guiyang, 550001, Guizhou, China.

Background: The Cathepsins family, including cathepsin B and cathepsin D, potentially affects the entire processes involved in atherosclerosis. Although coronary heart disease (CHD) has been widely studied as the basis of Sudden Cardiac Death (SCD), the relationship between CHD and CTSB/D remains unclear.

Methods: We screened for differentially expressed proteins (DEPs) associated with autophagy by limma package in R. Read More

View Article and Full-Text PDF

Melatonin prevents blood-retinal barrier breakdown and mitochondrial dysfunction in high glucose and hypoxia-induced in vitro diabetic macular edema model.

Toxicol In Vitro 2021 May 5;75:105191. Epub 2021 May 5.

Trakya University, Faculty of Medicine, Department of Medical Biology, Edirne, Turkey.

Diabetic macular edema (DME) is a leading cause of blindness in diabetic retinopathy. Prolonged hyperglycemia plus hypoxia contributes to DME pathogenesis. Retinal pigmented epithelial cells comprise the outer blood-retinal barrier and are essential for maintaining physiological functioning of the retina. Read More

View Article and Full-Text PDF

Electroacupuncture at GV20‑GB7 regulates mitophagy to protect against neurological deficits following intracerebral hemorrhage via inhibition of apoptosis.

Mol Med Rep 2021 Jul 6;24(1). Epub 2021 May 6.

Department of Clinical Medicine, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.

The acupuncture penetrating line of Baihui (GV20) to Qubin (GB7) spans the parietal, frontal and temporal lobes. The present study aimed to elucidate the mechanism by which electroacupuncture (EA) at GV20‑GB7 regulates mitophagy in intracerebral hemorrhage (ICH) and whether it serves a neuroprotective role. A whole blood‑induced ICH model was used. Read More

View Article and Full-Text PDF

Deficit of female sex hormones desensitizes rat cardiac mitophagy.

Chin J Physiol 2021 Mar-Apr;64(2):72-79

Department of Physiology, Faculty of Science, Mahidol University, Bangkok, Thailand.

Long-term deprivation of female sex hormones has been shown to mediate accumulation of damaged mitochondria in ventricular muscle leading to cardiovascular dysfunction. Therefore, the roles of female sex hormones in mitochondrial quality control are closely focused. In the present study, depletion of female sex hormones impairing mitochondrial autophagy in the heart was hypothesized. Read More

View Article and Full-Text PDF

Mitophagy reporter mouse analysis reveals increased mitophagy activity in disuse-induced muscle atrophy.

J Cell Physiol 2021 May 2. Epub 2021 May 2.

Department of Cellular Physiology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

Muscle disuse induces atrophy through increased reactive oxygen species (ROS) released from damaged mitochondria. Mitophagy, the autophagic degradation of mitochondria, is associated with increased ROS production. However, the mitophagy activity status during disuse-induced muscle atrophy has been a subject of debate. Read More

View Article and Full-Text PDF

BNIP3 promotes HIF-1α-driven melanoma growth by curbing intracellular iron homeostasis.

EMBO J 2021 May 1:e106214. Epub 2021 May 1.

Cell Death Research and Therapy Group, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.

BNIP3 is a mitophagy receptor with context-dependent roles in cancer, but whether and how it modulates melanoma growth in vivo remains unknown. Here, we found that elevated BNIP3 levels correlated with poorer melanoma patient's survival and depletion of BNIP3 in B16-F10 melanoma cells compromised tumor growth in vivo. BNIP3 depletion halted mitophagy and enforced a PHD2-mediated downregulation of HIF-1α and its glycolytic program both in vitro and in vivo. Read More

View Article and Full-Text PDF

Hypoxia-Driven HIF-1α Activation Reprograms Pre-Activated NK Cells towards Highly Potent Effector Phenotypes via ERK/STAT3 Pathways.

Cancers (Basel) 2021 Apr 15;13(8). Epub 2021 Apr 15.

Department of Biochemistry and Molecular Biology, College of Medicine, Korea University, Seoul 02841, Korea.

NK cells are the predominant innate lymphocyte subsets specialized to kill malignant tumor cells. In patients with advanced cancer, hypoxic stress shapes NK cells toward tumor-resistant and immunosuppressive phenotypes, hence a strategy to restore NK function is critical for successful tumor immunotherapy. Here, we present evidence that pre-activation and subsequent HIF-1α-dependent metabolic shift of NK cells from oxidative phosphorylation into glycolysis are keys to overcome hypoxia-mediated impairment in NK cell survival, proliferation, and tumor cytotoxicity. Read More

View Article and Full-Text PDF

Heparan Sulfate Deficiency in Cartilage: Enhanced BMP-Sensitivity, Proteoglycan Production and an Anti-Apoptotic Expression Signature after Loading.

Int J Mol Sci 2021 Apr 2;22(7). Epub 2021 Apr 2.

Research Centre for Experimental Orthopaedics, Orthopaedic University Hospital Heidelberg, 69118 Heidelberg, Germany.

Osteoarthritis (OA) represents one major cause of disability worldwide still evading efficient pharmacological or cellular therapies. Severe degeneration of extracellular cartilage matrix precedes the loss of mobility and disabling pain perception in affected joints. Recent studies showed that a reduced heparan sulfate (HS) content protects cartilage from degradation in OA-animal models of joint destabilization but the underlying mechanisms remained unclear. Read More

View Article and Full-Text PDF

LncRNA NEAT1 accelerates renal tubular epithelial cell damage by modulating mitophagy via miR-150-5p-Drp1 axis in diabetic nephropathy.

Exp Physiol 2021 Apr 29. Epub 2021 Apr 29.

Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, 410011, P.R. China.

New Findings: What is the central question of this study? Diabetic nephropathy (DN) is a severe diabetic complication correlated to higher mortality rate in diabetic patients. Renal tubular injury participates in the pathogenesis of DN. We aimed to uncover the biological function of NEAT1/miR-150-5p/Drp1 axis in an in vitro model of DN and elaborate the potential mechanisms. Read More

View Article and Full-Text PDF


Cardiovasc Res 2021 Apr 26. Epub 2021 Apr 26.

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center (MUMC), Maastricht, Netherlands.

Aims: Atherosclerotic plaque hypoxia is detrimental for macrophage function. Prolyl hydroxylases (PHDs) initiate cellular hypoxic responses, possibly influencing macrophage function in plaque hypoxia. Thus, we aimed to elucidate the role of myeloid PHDs in atherosclerosis. Read More

View Article and Full-Text PDF

Naringin protects H9C2 cardiomyocytes from chemical hypoxia‑induced injury by promoting the autophagic flux via the activation of the HIF‑1α/BNIP3 signaling pathway.

Int J Mol Med 2021 Jun 28;47(6). Epub 2021 Apr 28.

Department of Cardiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, P.R. China.

Naringin, a natural bioflavonoid, has been shown to exert protective effects in multiple cardiovascular diseases; however, the protective effects of naringin against hypoxic/ischemia‑induced myocardial are not yet fully understood. Autophagy is a vital factor involved in the pathogenesis of myocardial injury. The aim of the present study was to investigate the protective effects of naringin on H9c2 cells against chemical hypoxia [cobalt chloride (CoCl)]‑induced injury. Read More

View Article and Full-Text PDF

FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of BNIP3-mediated mitophagy.

Acta Pharmacol Sin 2021 Apr 20. Epub 2021 Apr 20.

Department of Neurosurgery, First Hospital of Jilin University, Changchun, 130021, China.

FOXO3a (forkhead box transcription factor 3a) is involved in regulating multiple biological processes in cancer cells. BNIP3 (Bcl-2/adenovirus E1B 19-kDa-interacting protein 3) is a receptor accounting for priming damaged mitochondria for autophagic removal. In this study we investigated the role of FOXO3a in regulating the sensitivity of glioma cells to temozolomide (TMZ) and its relationship with BNIP3-mediated mitophagy. Read More

View Article and Full-Text PDF

Short-Term High-Fat Feeding Does Not Alter Mitochondrial Lipid Respiratory Capacity but Triggers Mitophagy Response in Skeletal Muscle of Mice.

Front Endocrinol (Lausanne) 2021 31;12:651211. Epub 2021 Mar 31.

School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, United States.

Lipid overload of the mitochondria is linked to the development of insulin resistance in skeletal muscle which may be a contributing factor to the progression of type 2 diabetes during obesity. The targeted degradation of mitochondria through autophagy, termed mitophagy, contributes to the mitochondrial adaptive response to changes in dietary fat. Our previous work demonstrates long-term (2-4 months) consumption of a high-fat diet increases mitochondrial lipid oxidation capacity but does not alter markers of mitophagy in mice. Read More

View Article and Full-Text PDF

A New Trick for an Old Dog? Myocardial-Specific Roles for Prostaglandins as Mediators of Ischemic Injury and Repair.

Am J Physiol Heart Circ Physiol 2021 Apr 16. Epub 2021 Apr 16.

Department of Human Anatomy and Cell Science; College of Nursing in the Rady Faculty of Health Science, and The Diabetes Research Envisioned and Accomplished in Manitoba (DREAM); Children's Hospital Research Institute of Manitoba, University of Manitoba, Winnipeg, Canada.

The small lipid-derived paracrine signalling molecules known as prostaglandins have been recognized for their ability to modulate many facets of cardiovascular physiology since their initial discovery more than 85 years ago. While the role of prostaglandins in the vasculature has gained significant attention across time, a handful of historical studies have also directly implicated the cardiomyocyte in both prostaglandin synthesis and release. Recently our understanding of how prostaglandin receptor modulation impacts and contributes to myocardial structure and function has gained attention while leaving most other components of myocardial prostaglandin metabolism and signalling unexplored. Read More

View Article and Full-Text PDF

Alleviation of Inflammation and Oxidative Stress in Pressure Overload-Induced Cardiac Remodeling and Heart Failure via IL-6/STAT3 Inhibition by Raloxifene.

Oxid Med Cell Longev 2021 20;2021:6699054. Epub 2021 Mar 20.

Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Background: Inflammation and oxidative stress are involved in the initiation and progress of heart failure (HF). However, the role of the IL6/STAT3 pathway in the pressure overload-induced HF remains controversial.

Methods And Results: Transverse aortic constriction (TAC) was used to induce pressure overload-HF in C57BL/6J mice. Read More

View Article and Full-Text PDF

Muscle Proteomic Profile before and after Enzyme Replacement Therapy in Late-Onset Pompe Disease.

Int J Mol Sci 2021 Mar 11;22(6). Epub 2021 Mar 11.

Department of Biomedical Sciences for Health, University of Milan, 20090 Milano, Italy.

Mutations in the acidic alpha-glucosidase (GAA) coding gene cause Pompe disease. Late-onset Pompe disease (LOPD) is characterized by progressive proximal and axial muscle weakness and atrophy, causing respiratory failure. Enzyme replacement therapy (ERT), based on recombinant human GAA infusions, is the only available treatment; however, the efficacy of ERT is variable. Read More

View Article and Full-Text PDF

Ascorbate uptake enables tubular mitophagy to prevent septic AKI by PINK1-PARK2 axis.

Biochem Biophys Res Commun 2021 May 31;554:158-165. Epub 2021 Mar 31.

Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, PR China. Electronic address:

Ascorbate (Vitamin C) has been proposed as a promising therapeutic agent against sepsis in clinical trials, but there is little experimental evidence on its anti-septic efficacy. We report that Toll-like receptor 4 (TLR4) activation by LPS stimuli augments ascorbate uptake in murine and human tubular cells through upregulation of two ascorbate transporters SVCT-1 and -2 mediated by Fn14/SCF cascade. Ascorbate restriction, or knockout of SVCT-1 and -2, the circumstance reminiscent to blockade of ascorbate uptake, endows tubular cells more vulnerable to the LPS-inducible apoptosis, whereas exogenous administration of ascorbate overrides the ruin execution, for which the PINK1-PARK2, rather than BNIP3-NIX axis is required. Read More

View Article and Full-Text PDF

EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma.

Cell Death Dis 2021 Apr 1;12(4):344. Epub 2021 Apr 1.

Department of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.

Studies have indicated that dysfunction of autophagy is involved in the initiation and progression of multiple tumors and their chemoradiotherapy. Epstein-Barr virus (EBV) is a lymphotropic human gamma herpes virus that has been implicated in the pathogenesis of nasopharyngeal carcinoma (NPC). EBV encoded latent membrane protein1 (LMP1) exhibits the properties of a classical oncoprotein. Read More

View Article and Full-Text PDF

Synergistic Effect of Apigenin and Curcumin on Apoptosis, Paraptosis and Autophagy-related Cell Death in HeLa Cells.

Anticancer Res 2021 Mar;41(3):1271-1282

Department of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey;

Background/aim: We aimed to investigate the synergistic effects of apigenin and curcumin on the cross-talk between apoptosis and autophagic cell death, as well as on paraptosis in HeLa cells.

Materials And Methods: Cell viability was measured using the MTT assay. Synergistic effects were measured using the Bliss independence model. Read More

View Article and Full-Text PDF

Triptolide prevents lipopolysaccharide-induced skeletal muscle atrophy via inhibiting NF-κB/TNF-α and regulating protein synthesis/degradation pathway.

Br J Pharmacol 2021 Mar 31. Epub 2021 Mar 31.

Department of Pharmacology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

Background And Purpose: Increasing evidence suggests systemic inflammation-caused skeletal muscle atrophy as a major clinical feature of cachexia. Triptolide obtained from Tripterygium wilfordii Hook F possesses potent anti-inflammatory and immunosuppressive effects. The present study aims to evaluate the protective effects and molecular mechanisms of triptolide on inflammation-induced skeletal muscle atrophy. Read More

View Article and Full-Text PDF

STK3/STK4 signalling in adipocytes regulates mitophagy and energy expenditure.

Nat Metab 2021 03 23;3(3):428-441. Epub 2021 Mar 23.

College of Pharmacy, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.

Obesity reduces adipocyte mitochondrial function, and expanding adipocyte oxidative capacity is an emerging strategy to improve systemic metabolism. Here, we report that serine/threonine-protein kinase 3 (STK3) and STK4 are key physiological suppressors of mitochondrial capacity in brown, beige and white adipose tissues. Levels of STK3 and STK4, kinases in the Hippo signalling pathway, are greater in white than brown adipose tissues, and levels in brown adipose tissue are suppressed by cold exposure and greatly elevated by surgical denervation. Read More

View Article and Full-Text PDF

Exercise combined with trimetazidine improves anti-fatal stress capacity through enhancing autophagy and heat shock protein 70 of myocardium in mice.

Int J Med Sci 2021 6;18(7):1680-1686. Epub 2021 Feb 6.

Division of Cardiac Rehabilitation, Department of Physical Medicine & Rehabilitation, Xiangya Hospital Central South University, Changsha, Hunan 410008, P.R China.

Anti-stress capacity is important to resist the occurrence of adverse events. To observe the effects of exercise, trimetazidine alone or combined on the anti-stress capacity of mice, and further explore its potential mechanism. Forty-four C57BL/6 male mice aged 8 weeks were randomly divided into four groups (n=11 for each group): control group (group C), exercise group (group E), trimetazidine group (group T), exercise combined with trimetazidine group (group TE). Read More

View Article and Full-Text PDF
February 2021

Markers of muscle atrophy and impact of treatment with pergolide in horses with pituitary pars intermedia dysfunction and muscle atrophy.

Domest Anim Endocrinol 2021 Feb 18;76:106620. Epub 2021 Feb 18.

School of Veterinary Medicine, Texas Tech University, Amarillo, TX 79106, USA.

Pituitary pars intermedia dysfunction (PPID) is a common endocrine disorder of aged horses, with muscle atrophy as one of the clinical signs. We sought to compare muscle mass and regulation of skeletal muscle proteolysis between horses with PPID and muscle atrophy to older horses without PPID, and to assess the impact of treatment with pergolide (dopaminergic agonist) on PPID horses. We hypothesized that PPID-associated muscle atrophy is a result of increased proteolysis, and that markers of muscle atrophy and proteolysis would improve over time with pergolide treatment. Read More

View Article and Full-Text PDF
February 2021

Mitophagy in Pancreatic Cancer.

Front Oncol 2021 26;11:616079. Epub 2021 Feb 26.

Department of Surgery, UT Southwestern Medical Center, Dallas, TX, United States.

Pancreatic ductal adenocarcinoma (PDAC), one of the most aggressive solid malignancies, is characterized by the presence of oncogenic KRAS mutations, poor response to current therapies, prone to metastasis, and a low 5-year overall survival rate. Macroautophagy (herein referred to as autophagy) is a lysosome-dependent degradation system that forms a series of dynamic membrane structures to engulf, degrade, and recycle various cargoes, such as unused proteins, damaged organelles, and invading pathogens. Autophagy is usually upregulated in established cancers, but it plays a dual role in the regulation of the initiation and progression of PDAC. Read More

View Article and Full-Text PDF
February 2021

Hypoxic training upregulates mitochondrial turnover and angiogenesis of skeletal muscle in mice.

Life Sci 2021 Mar 11:119340. Epub 2021 Mar 11.

School of Physical Education and Sport Training, Shanghai University of Sport, Changhai road 399, Yangpu District, Shanghai 200438, China. Electronic address:

Aims: Hypoxic training promotes human cardiopulmonary function and exercise performance efficiently, but the myocellular mechanism has been less studied. We aimed to examine the effects of hypoxic trainings on mitochondrial turnover and vascular remodeling of skeletal muscle.

Main Methods: C57BL/6 J mice were divided into control, hypoxic exposure, exercise training, "live high-train low" (LHTL), and "live low-train high" (LLTH) groups (n = 8/group). Read More

View Article and Full-Text PDF

ROS-dependent HIF1α activation under forced lipid catabolism entails glycolysis and mitophagy as mediators of higher proliferation rate in cervical cancer cells.

J Exp Clin Cancer Res 2021 Mar 11;40(1):94. Epub 2021 Mar 11.

Department of Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133, Rome, Italy.

Background: In the last decades, the concept of metabolic rewiring as a cancer hallmark has been expanded beyond the "Warburg effect" and the importance of other metabolic routes, including lipid metabolism, has emerged. In cancer, lipids are not only a source of energy but are also required for the formation of membranes building blocks, signaling and post-translational modification of proteins. Since lipid metabolism contributes to the malignancy of cancer cells, it is an attractive target for therapeutic strategies. Read More

View Article and Full-Text PDF

KCa3.1 Mediates Dysregulation of Mitochondrial Quality Control in Diabetic Kidney Disease.

Front Cell Dev Biol 2021 19;9:573814. Epub 2021 Feb 19.

Kolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.

Mitochondrial dysfunction is implicated in the pathogenesis of diabetic kidney disease. Mitochondrial quality control is primarily mediated by mitochondrial turnover and repair through mitochondrial fission/fusion and mitophagy. We have previously shown that blockade of the calcium-activated potassium channel KCa3. Read More

View Article and Full-Text PDF
February 2021

Circular RNA POSTN Promotes Myocardial Infarction-Induced Myocardial Injury and Cardiac Remodeling by Regulating miR-96-5p/BNIP3 Axis.

Front Cell Dev Biol 2020 18;8:618574. Epub 2021 Feb 18.

Department of Cardiovascular Surgery, PLA General Hospital, Beijing, China.

Myocardial infarction (MI) is the most prevalent cardiac disease with high mortality, leading to severe heart injury. Circular RNAs (circRNAs) are a new type of regulatory RNAs and participate in multiple pathological cardiac progressions. However, the role of circRNAs Postn (circPostn) in MI modulation remains unclear. Read More

View Article and Full-Text PDF
February 2021