Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health DOI Creative Commons
Ne N. Wu, Haili Tian, Peijie Chen

et al.

Cells, Journal Year: 2019, Volume and Issue: 8(11), P. 1436 - 1436

Published: Nov. 14, 2019

Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. may positively affect risk factors including body weight, blood pressure, insulin sensitivity, lipid glucose metabolism, heart function, endothelial fat composition. With ever-rising prevalence obesity other types metabolic as well sedentary lifestyle, regular moderate intensity has been indicated to benefit health reduce overall disease mortality. Exercise offers a wide cadre favorable responses system such improved dynamics system, reduced coronary diseases cardiomyopathies, enhanced cardiac reserve capacity, autonomic regulation. Ample clinical experimental evidence an emerging role autophagy, conservative catabolism process degrade recycle cellular organelles nutrients, training-offered benefits. Regular physical unique form physiological stress capable triggering adaptation while autophagy selective seems be permissive adaptation. Here this mini-review, we will summarize mitochondrial namely mitophagy versus on function.

Language: Английский

Biological Functions of Autophagy Genes: A Disease Perspective DOI Creative Commons
Beth Levine, Guido Kroemer

Cell, Journal Year: 2019, Volume and Issue: 176(1-2), P. 11 - 42

Published: Jan. 1, 2019

Language: Английский

Citations

2281

Autophagy in major human diseases DOI Creative Commons
Daniel J. Klionsky, Giulia Petroni, Ravi K. Amaravadi

et al.

The EMBO Journal, Journal Year: 2021, Volume and Issue: 40(19)

Published: Aug. 30, 2021

Review30 August 2021Open Access Autophagy in major human diseases Daniel J Klionsky orcid.org/0000-0002-7828-8118 Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA Search for more papers by this author Giulia Petroni Department Radiation Oncology, Weill Cornell Medical College, New York, NY, Ravi K Amaravadi Medicine, Pennsylvania, Philadelphia, PA, Abramson Cancer Center, Eric H Baehrecke Molecular, Cell and Biology, Massachusetts School, Worcester, MA, Andrea Ballabio orcid.org/0000-0003-1381-4604 Telethon Institute Genetics Pozzuoli, Italy Translational Sciences, Section Pediatrics, Federico II University, Naples, Molecular Human Genetics, Baylor College Jan Dan Duncan Neurological Research Texas Children Hospital, Houston, TX, Patricia Boya orcid.org/0000-0003-3045-951X Margarita Salas Center Biological Research, Spanish National Council, Madrid, Spain José Manuel Bravo-San Pedro Faculty Physiology, Complutense Networked Biomedical Neurodegenerative Diseases (CIBERNED), Ken Cadwell Kimmel Biology Medicine at the Skirball York Grossman School Microbiology, Division Gastroenterology Hepatology, Langone Health, Francesco Cecconi orcid.org/0000-0002-5614-4359 Stress Survival Unit, Autophagy, Recycling Disease (CARD), Danish Society Copenhagen, Denmark Pediatric Onco-Hematology Gene Therapy, IRCCS Bambino Gesù Children's Rome, Rome 'Tor Vergata', Augustine M Choi Pulmonary Critical Care Joan Sanford I. York-Presbyterian Mary E Nephrology Hypertension, Charleen T Chu orcid.org/0000-0002-5052-8271 Pathology, Pittsburgh Pittsburgh, Patrice Codogno orcid.org/0000-0002-5492-3180 Institut Necker-Enfants Malades, INSERM U1151-CNRS UMR 8253, Paris, France Université de Maria Isabel Colombo Laboratorio Mecanismos Moleculares Implicados en el Tráfico Vesicular y la Autofagia-Instituto Histología Embriología (IHEM)-Universidad Nacional Cuyo, CONICET- Facultad Ciencias Médicas, Mendoza, Argentina Ana Cuervo orcid.org/0000-0002-0771-700X Developmental Albert Einstein Bronx, Aging Studies, Vojo Deretic Inflammation Metabolism (AIM, Excellence, Mexico Health Albuquerque, NM, Ivan Dikic orcid.org/0000-0001-8156-9511 Biochemistry II, Goethe Frankfurt, Frankfurt am Main, Germany Buchmann Zvulun Elazar Biomolecular The Weizmann Science, Rehovot, Israel Eeva-Liisa Eskelinen Biomedicine, Turku, Finland Gian Fimia orcid.org/0000-0003-4438-3325 Sapienza Epidemiology, Preclinical Advanced Diagnostics, Infectious 'L. Spallanzani' IRCCS, David A Gewirtz orcid.org/0000-0003-0437-4934 Pharmacology Toxicology, Virginia Commonwealth Richmond, VA, Douglas R Green Immunology, St. Jude Memphis, TN, Malene Hansen Burnham Prebys Discovery Program Development, Aging, Regeneration, La Jolla, CA, Marja Jäättelä orcid.org/0000-0001-5950-7111 Death Metabolism, & Disease, Cellular Terje Johansen orcid.org/0000-0003-1451-9578 Group, Tromsø—The Arctic Norway, Tromsø, Norway Gábor Juhász Szeged, Hungary Anatomy, Eötvös Loránd Budapest, Vassiliki Karantza Merck Co., Inc., Kenilworth, NJ, Claudine Kraft orcid.org/0000-0002-3324-4701 ZBMZ, Freiburg, CIBSS - Centre Integrative Signalling Guido Kroemer orcid.org/0000-0002-9334-4405 Recherche des Cordeliers, Equipe Labellisée par Ligue Contre le Cancer, Sorbonne Université, Inserm U1138, Universitaire France, Metabolomics Platforms, Gustave Roussy, Villejuif, Pôle Biologie, Hôpital Européen Georges Pompidou, AP-HP, Suzhou Systems Chinese Academy Suzhou, China Karolinska Women's Stockholm, Sweden Nicholas Ktistakis Programme, Babraham Cambridge, UK Sharad Kumar orcid.org/0000-0001-7126-9814 South Australia, Adelaide, SA, Australia Carlos Lopez-Otin orcid.org/0000-0001-6964-1904 Departamento Bioquímica Biología Medicina, Instituto Universitario Oncología del Principado Asturias (IUOPA), Universidad Oviedo, Centro Investigación Biomédica Red Cáncer (CIBERONC), Kay F Macleod Ben May Gordon W-338, Chicago, IL, Frank Madeo Biosciences, NAWI Graz, Austria BioTechMed-Graz, Field Excellence BioHealth – Jennifer Martinez Immunity, Laboratory, Environmental NIH, Triangle Park, NC, Alicia Meléndez Department, Queens City Flushing, Graduate PhD Programs Noboru Mizushima orcid.org/0000-0002-6258-6444 Tokyo, Japan Christian Münz orcid.org/0000-0001-6419-1940 Viral Immunobiology, Experimental Zurich, Switzerland Josef Penninger Biotechnology Austrian (IMBA), Vienna BioCenter (VBC), Vienna, British Columbia, Vancouver, BC, Canada Rushika Perera orcid.org/0000-0003-2435-2273 California, San Francisco, Helen Diller Family Comprehensive Mauro Piacentini orcid.org/0000-0003-2919-1296 "Tor Vergata", Laboratory Cytology Russian Saint Petersburg, Russia Fulvio Reggiori orcid.org/0000-0003-2652-2686 Cells Systems, Section, Groningen, Netherlands C Rubinsztein Cambridge Dementia Kevin Ryan Beatson Glasgow, Junichi Sadoshima Cardiovascular Rutgers Jersey Newark, Laura Santambrogio Sandra Edward Meyer Caryl Englander Precision Luca Scorrano orcid.org/0000-0002-8515-8928 Istituto Veneto di Medicina Molecolare, Padova, Hans-Uwe Simon Pharmacology, Bern, Clinical Immunology Allergology, Sechenov Moscow, Fundamental Kazan Federal Kazan, Anna Katharina Kennedy Rheumatology, NDORMS, Oxford, Anne Simonsen orcid.org/0000-0003-4711-7057 Basic Oslo, Reprogramming, Oslo Hospital Montebello, Alexandra Stolz orcid.org/0000-0002-3340-439X Nektarios Tavernarakis orcid.org/0000-0002-5253-1466 Biotechnology, Foundation Technology-Hellas, Heraklion, Crete, Greece Sharon Tooze orcid.org/0000-0002-2182-3116 Francis Crick London, Tamotsu Yoshimori orcid.org/0000-0001-9787-3788 Osaka Suita, Intracellular Membrane Dynamics, Frontier Integrated Science Division, Open Transdisciplinary Initiatives (OTRI), Junying Yuan Interdisciplinary on Chemistry, Shanghai Organic Shanghai, Harvard Boston, Zhenyu Yue Neurology, Friedman Brain Icahn Mount Sinai, Qing Zhong orcid.org/0000-0001-6979-955X Key Differentiation Apoptosis Ministry Education, Pathophysiology, Jiao Tong (SJTU-SM), Lorenzo Galluzzi Corresponding Author [email protected] orcid.org/0000-0003-2257-8500 Dermatology, Yale Haven, CT, Pietrocola orcid.org/0000-0002-2930-234X Biosciences Nutrition, Huddinge, mor

Language: Английский

Citations

1092

Adipose tissue and insulin resistance in obese DOI Open Access
Bulbul Ahmed, Rifat Sultana, Michael W. Greene

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2021, Volume and Issue: 137, P. 111315 - 111315

Published: Feb. 7, 2021

Currently, obesity has become a global health issue and is referred to as an epidemic. Dysfunctional obese adipose tissue plays pivotal role in the development of insulin resistance. However, mechanism how dysfunctional obese-adipose develops insulin-resistant circumstances remains poorly understood. Therefore, this review attempts highlight potential mechanisms behind obesity-associated Multiple risk factors are directly or indirectly associated with increased obesity; among them, environmental factors, genetics, aging, gut microbiota, diets prominent. Once individual becomes obese, adipocytes increase their size; therefore, tissues larger dysfunctional, recruit macrophages, then these polarize pro-inflammatory states. Enlarged release excess free fatty acids (FFAs), reactive oxygen species (ROS), cytokines. Excess systemic FFAs dietary lipids enter inside cells non-adipose organs such liver, muscle, pancreas, deposited ectopic fat, generating lipotoxicity. Toxic dysregulate cellular organelles, e.g., mitochondria, endoplasmic reticulum, lysosomes. Dysregulated organelles ROS pro-inflammation, resulting inflammation. Long term low-grade inflammation prevents from its action signaling pathway, disrupts glucose homeostasis, results dysregulation. Overall, long-term overnutrition develop into resistance chronic through lipotoxicity, creating clinical conditions. This also shows that liver most sensitive organ undergoing impairment faster than other organs, thus, hepatic primary event leads subsequent peripheral

Language: Английский

Citations

575

Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases DOI
Jun Ren, Yaguang Bi, James R. Sowers

et al.

Nature Reviews Cardiology, Journal Year: 2021, Volume and Issue: 18(7), P. 499 - 521

Published: Feb. 22, 2021

Language: Английский

Citations

482

Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments DOI Creative Commons

Rexiati Ruze,

Tiantong Liu,

Xi Zou

et al.

Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14

Published: April 21, 2023

The prevalence of obesity and diabetes mellitus (DM) has been consistently increasing worldwide. Sharing powerful genetic environmental features in their pathogenesis, amplifies the impact susceptibility factors on DM. ectopic expansion adipose tissue excessive accumulation certain nutrients metabolites sabotage metabolic balance via insulin resistance, dysfunctional autophagy, microbiome-gut-brain axis, further exacerbating dysregulation immunometabolism through low-grade systemic inflammation, leading to an accelerated loss functional β-cells gradual elevation blood glucose. Given these intricate connections, most available treatments type 2 DM (T2DM) have a mutual effect each other. For example, anti-obesity drugs can be anti-diabetic some extent, medicines, contrast, shown increase body weight, such as insulin. Meanwhile, surgical procedures, especially bariatric surgery, are more effective for both T2DM. Besides guaranteeing availability accessibility all diagnostic therapeutic tools, clinical experimental investigations pathogenesis two diseases warranted improve efficacy safety newly developed treatments.

Language: Английский

Citations

326

Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications DOI
Jun Ren, Ne N. Wu, Shuyi Wang

et al.

Physiological Reviews, Journal Year: 2021, Volume and Issue: 101(4), P. 1745 - 1807

Published: May 5, 2021

The prevalence of heart failure is on the rise and imposes a major health threat, in part, due to rapidly increased overweight obesity. To this point, epidemiological, clinical, experimental evidence supports existence unique disease entity termed "obesity cardiomyopathy," which develops independent hypertension, coronary disease, other diseases. Our contemporary review evaluates for pathological condition, examines putative responsible mechanisms, discusses therapeutic options disorder. Clinical findings have consolidated presence left ventricular dysfunction Experimental investigations uncovered pathophysiological changes myocardial structure function genetically predisposed diet-induced Indeed, consolidates wide array cellular molecular mechanisms underlying etiology obesity cardiomyopathy including adipose tissue dysfunction, systemic inflammation, metabolic disturbances (insulin resistance, abnormal glucose transport, spillover free fatty acids, lipotoxicity, amino acid derangement), altered intracellular especially mitochondrial Ca2+ homeostasis, oxidative stress, autophagy/mitophagy defect, fibrosis, dampened flow reserve, microvascular (microangiopathy), endothelial impairment. Given important role risk failure, that with preserved systolic recent rises COVID-19-associated cardiovascular mortality, should provide compelling cardiomyopathy, various comorbid conditions, offer new insights into potential approaches (pharmacological lifestyle modification) clinical management cardiomyopathy.

Language: Английский

Citations

252

Targeting Autophagy in Aging and Aging-Related Cardiovascular Diseases DOI Creative Commons
Jun Ren, Yingmei Zhang

Trends in Pharmacological Sciences, Journal Year: 2018, Volume and Issue: 39(12), P. 1064 - 1076

Published: Oct. 26, 2018

Language: Английский

Citations

231

The ménage à trois of autophagy, lipid droplets and liver disease DOI Creative Commons
Yasmina Filali-Mouncef, Catherine J. Hunter,

Federica Roccio

et al.

Autophagy, Journal Year: 2021, Volume and Issue: 18(1), P. 50 - 72

Published: April 2, 2021

Autophagic pathways cross with lipid homeostasis and thus provide energy essential building blocks that are indispensable for liver functions. Energy deficiencies compensated by breaking down droplets (LDs), intracellular organelles store neutral lipids, in part a selective type of autophagy, referred to as lipophagy. The process lipophagy does not appear be properly regulated fatty diseases (FLDs), an important risk factor the development hepatocellular carcinomas (HCC). Here we overview on our current knowledge biogenesis functions LDs, mechanisms underlying their lysosomal turnover autophagic processes. This review also focuses nonalcoholic steatohepatitis (NASH), specific FLD characterized steatosis, chronic inflammation cell death. Particular attention is paid role macroautophagy macrolipophagy relation parenchymal non-parenchymal cells NASH, this disease has been associated inappropriate various types liver.Abbreviations: ACAT: acetyl-CoA acetyltransferase; ACAC/ACC: carboxylase; AKT: AKT serine/threonine kinase; ATG: autophagy related; AUP1: AUP1 droplet regulating VLDL assembly factor; BECN1/Vps30/Atg6: beclin 1; BSCL2/seipin: BSCL2 associated, seipin; CMA: chaperone-mediated autophagy; CREB1/CREB: cAMP responsive element binding protein CXCR3: C-X-C motif chemokine receptor 3; DAGs: diacylglycerols; DAMPs: danger/damage-associated molecular patterns; DEN: diethylnitrosamine; DGAT: diacylglycerol O-acyltransferase; DNL: de novo lipogenesis; EHBP1/NACSIN (EH domain 1); EHD2/PAST2: EH containing 2; CoA: coenzyme A; CCL/chemokines: ligands; CCl4: carbon tetrachloride; ER: endoplasmic reticulum; ESCRT: endosomal sorting complexes required transport; FA: acid; FFAs: free acids; FFC: high saturated fats, fructose cholesterol; FGF21: fibroblast growth 21; FITM/FIT: fat storage inducing transmembrane protein; FLD: diseases; FOXO: forkhead box O; GABARAP: GABA A receptor-associated GPAT: glycerol-3-phosphate acyltransferase; HCC: carcinoma; HDAC6: histone deacetylase 6; HECT: homologous E6-AP C-terminus; HFCD: fat, choline deficient; HFD: high-fat diet; HSCs: hepatic stellate cells; HSPA8/HSC70: heat shock family (Hsp70) member 8; ITCH/AIP4: itchy E3 ubiquitin ligase; KCs: Kupffer LAMP2A: membrane 2A; LDs: droplets; LDL: low density lipoprotein; LEP/OB: leptin; LEPR/OBR: leptin receptor; LIPA/LAL: lipase A, acid type; LIPE/HSL: E, hormone sensitive LIR: LC3-interacting region; LPS: lipopolysaccharide; LSECs: sinusoidal endothelial MAGs: monoacylglycerols; MAPK: mitogen-activated MAP3K5/ASK1: kinase 5; MAP1LC3/LC3: microtubule 1 light chain MCD: methionine-choline MGLL/MGL: monoglyceride lipase; MLXIPL/ChREBP: MLX interacting like; MTORC1: mechanistic target rapamycin complex NAFLD: disease; NAS: NAFLD activity score; NASH: steatohepatitis; NPC: NPC cholesterol transporter; NR1H3/LXRα: nuclear subfamily group H NR1H4/FXR: 4; PDGF: platelet derived PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit PLIN: perilipin; PNPLA: patatin like phospholipase containing; PNPLA2/ATGL: PNPLA3/adiponutrin: PPAR: peroxisome proliferator activated PPARA/PPARα: alpha; PPARD/PPARδ: delta; PPARG/PPARγ: gamma; PPARGC1A/PGC1α: PPARG coactivator PRKAA/AMPK: AMP-activated subunit; PtdIns3K: class III 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase tensin homolog; ROS: reactive oxygen species; SE: sterol esters; SIRT1: sirtuin SPART/SPG20: spartin; SQSTM1/p62: sequestosome SREBF1/SREBP1c: regulatory transcription TAGs: triacylglycerols; TFE3: IGHM enhancer TFEB: EB; TGFB1/TGFβ: transforming beta Ub: ubiquitin; UBE2G2/UBC7: conjugating enzyme E2 G2; ULK1/Atg1: unc-51 activating USF1: upstream VLDL: very-low VPS: vacuolar sorting; WIPI: WD-repeat domain, phosphoinositide interacting; WDR: WD repeat domain.

Language: Английский

Citations

225

Targeting autophagy in ischemic stroke: From molecular mechanisms to clinical therapeutics DOI Creative Commons
Amir Ajoolabady,

Shuyi Wang,

Guido Kroemer

et al.

Pharmacology & Therapeutics, Journal Year: 2021, Volume and Issue: 225, P. 107848 - 107848

Published: April 4, 2021

Language: Английский

Citations

215

The FoxO–Autophagy Axis in Health and Disease DOI
Zhiyong Cheng

Trends in Endocrinology and Metabolism, Journal Year: 2019, Volume and Issue: 30(9), P. 658 - 671

Published: Aug. 20, 2019

Language: Английский

Citations

195