Abstracts tagged "autophagy"

Abstract Number: 1434 • 2017 ACR/ARHP Annual Meeting
COX-2 Inhibitor Contributes Cell Death in Rheumatoid Arthritis Fibroblast-like Synoviocytes Via PI3K/AKT/mTOR Signaling Pathway Triggered By Autophagy
Sang-Hyon Kim¹, Jihye Bang², Ji-Min Kim¹, Chang-Nam Son¹, Jin-Nyeong Chae¹ and Hye-Jin Jeong³, ¹Division of Rheumatology, Department of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Republic of Korea, Daegu, Korea, Republic of (South), ²Division of Rheumatology, Department of Internal Medicine, Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea, Republic of (South), ³Department of Rheumatology, Keimyung University Dongsan Medical Center, Daegu, Korea, Republic of (South)
Background/Purpose: Recently, the possibilities that autophagy regulates apoptosis resistance and hyperplasia of fibroblast-like synoviocytes (FLS) were also presented. The aim of this study is to…
Abstract Number: 1745 • 2017 ACR/ARHP Annual Meeting
Autophagic Memory in Stress Experienced Human T Cells
Pavanish Kumar¹, Jorg van Loosdregt², Suzan Saidin¹, Bhairav Paleja¹ and Salvatore Albani¹, ¹SingHealth Translational Immunology and Inflammation Centre (STIIC), Duke-NUS Medical School, Singapore, Singapore, ²Laboratory for Translational immunology, University Medical Center Utrecht, Utrecht, Netherlands
Background/Purpose: Autophagy is central to many key immune related pathways, disregulation of which has been associated with rheumatoid arthritis (RA), cancer and neurodegenerative diseases. Autophagy…
Abstract Number: 1925 • 2017 ACR/ARHP Annual Meeting
TGFβ Promotes Fibrosis By MYST1-Dependent Epigenetic Regulation of Autophagy
Ariella Zehender¹, Neng-Yu Lin², Adrian Stefanica³, Chih-Wei Chen⁴, Alina Soare⁵, Thomas Wohlfahrt⁶, Simon Rauber⁶, Christina Bergmann⁷, Andreas Ramming⁸, Oliver Distler⁹, Georg Schett¹⁰ and Jörg Distler⁵, ¹1Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany, ²Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, ³1Department of Internal Medicine 3 – Rheumatology and Immunology, University of Erlangen, Erlangen, Germany, ⁴Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany, Erlangen, Germany, ⁵Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany, ⁶Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany, ⁷Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany, ⁸Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany, ⁹Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland, ¹⁰Department of Internal Medicine 3 – Rheumatology and Immunology, Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany
Background/Purpose: Autophagy (Atg) is catabolic process allowing cells to degrade unnecessary or dysfunctional cellular organelles. Aberrant activation of Atg has been implicated into the pathogenesis…
Abstract Number: 1926 • 2017 ACR/ARHP Annual Meeting
Cardiac Remodeling in Systemic Sclerosis: TGF-β/Fra2-Dependent Autophagy As a Novel Target for Heart Fibrosis
Mara Stellato¹, Michal Rudnik¹, Florian Renoux¹, Elena Pachera¹, Karl Sotlar², Karin Klingel³, Joerg C. Henes⁴, Przemyslaw Blyszczuk^1,5, Oliver Distler¹ and Gabriela Kania¹, ¹Department of Rheumatology, Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland, ²Institute of Pathology, Ludwig Maximilians University, Munich, Germany, ³Department of Molecular Pathology, University Hospital Tuebingen, Tuebingen, Germany, ⁴Department of Internal Medicine II, Division of Rheumatology, University Hospital Tuebingen, Tuebingen, Germany, ⁵Department of Clinical Immunology, Jagiellonian University Medical College, Krakow, Poland
Background/Purpose: SSc patients frequently suffer from primary cardiac involvement. The main histological feature is fibrosis, but the mechanisms responsible for the heart failure remain unclear.…
Abstract Number: 1931 • 2017 ACR/ARHP Annual Meeting
Targeting Cartilage Aging As Osteoarthritis Therapeutics By Drug Repurposing
Beatriz Carames¹, Uxia Nogueira-Recalde², Maria I. Loza³, Francisco J Blanco² and Eduardo Dominguez⁴, ¹Cartilage Biology Group. Rheumatology Division, INIBIC–CHUAC, A Coruña, A Coruña, Spain, ²Cartilage Biology Group. Rheumatology Division, INIBIC-CHUAC, A Coruña, A Coruña, Spain, ³BioFarma Research Group. University of Santiago de Compostela, santiago de Compostela, Spain, ⁴BioFarma Research Group. University of Santiago de Compostela, Santiago de Compostela, Spain
Background/Purpose: Background: Effective treatments for Osteoarthritis (OA) are not available. In aging-related diseases, including OA, failure of cellular homeostasis mechanisms, such as autophagy can cause…
Abstract Number: 2698 • 2017 ACR/ARHP Annual Meeting
IL-21-mTOR Axis Blocks the Differentiation and Function of SLE Tregs Via Suppression of Autophagy
Hiroshi Kato¹ and Andras Perl², ¹Division of Rheumatology/Internal Medicine, SUNY Upstate Medical University, Syracuse, NY, ²Dept of Medicine, SUNY Upstate Medical University, Syracuse, NY
Background/Purpose: Mechanistic target of rapamycin (mTOR) activation has emerged as a prominent mediator of pro-inflammatory T-cell expansion and regulatory T (Treg) cell depletion in systemic…
Abstract Number: 2705 • 2016 ACR/ARHP Annual Meeting
Decreased Expression of Autophagy Genes and Their Association with Spinal Damage in Patients with Ankylosing Spondylitis
Min-Chan Park¹, Hye Won Kim², Jason Jungsik Song¹ and Yong-Beom Park¹, ¹Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea, ²Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea
Background/Purpose: However, a role of autophagy in ankylosing spondylitis has not been clearly elucidated and the association of autophagy-related gene expression levels with inflammatory or…
Abstract Number: 2128 • 2016 ACR/ARHP Annual Meeting
Autophagic Clearance of Dysfunctional Mitochondria Requires Parkin in Human Chondrocytes
Mohammad Y Ansari¹ and Tariq M. Haqqi², ¹Anatomy & Neurobiology, Northeast Ohio Medical University, Roostown, OH, ²Anatomy & Neurobiology, Northeast Ohio Medical University, Rootstown, OH
Background/Purpose:
Abstract Number: 2132 • 2016 ACR/ARHP Annual Meeting
Deficient Autophagy Induces Premature Senescence in Aging and Osteoarthritis
Beatriz Carames¹, Paloma Lopez de Figueroa¹, Madalena Ribeiro¹, Valentina Calamia², Fernando Osorio³, Carlos Lopez-Otin³ and Francisco J. Blanco^1,4, ¹Cartilage Biology Group. Rheumatology Division, INIBIC-Hospital Universitario A Coruña, A Coruña, Spain, ²Osteoarticular and Aging Research Lab. Proteomics Unit - Associated Node to ProteoRed, Rheumatology Division, Proteomics Group-ProteoRed/ISCIII, INIBIC-CHUAC, A Coruña, Spain, ³Degradome Lab, Universidad de Oviedo, Oviedo, Spain, ⁴Rheumatology Division, INIBIC-Complejo Hospitalario Universitario A Coruña (CHUAC), La Coruña, Spain
Background/Purpose: Previous findings indicated that autophagy is defective in Aging and Osteoarthritis (OA). Autophagy is essential to maintain chondrocyte homeostasis by regulating the intracellular macromolecule…
Abstract Number: 1128 • 2015 ACR/ARHP Annual Meeting
Insulin-Induced Cartilage Degradation in Osteoarthritis Is Associated to Defective Autophagy
Beatriz Carames¹, Madalena Ribeiro^1,2, Paloma Lopez de Figueroa¹, Alexandrina Mendes² and Francisco J. Blanco¹, ¹Cartilage Biology Group. Rheumatology Division, INIBIC-Hospital Universitario A Coruña, A Coruña, Spain, ²Centre for Neuroscience and Cell Biology, University of Coimbra; Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal
Background/Purpose: Autophagy, a key cellular quality control mechanism, is defective in Osteoarthritis (OA) and Type 2 Diabetes (T2D). T2D has been proposed as a risk…
Abstract Number: 1146 • 2015 ACR/ARHP Annual Meeting
Deficiency of TLR2 and TLR4 Impairs Autophagic Flux in Chondrocytes
Yun Wang¹, Robert Terkeltaub² and Ru Liu-Bryan³, ¹Medicine-Rheumatology, VA Medical Ctr/UCSD, San Diego, CA, ²Medicine-Rheumatology, VA Medical Ctr/University of California San Diego, San Diego, CA, ³Medicine-Rheumatology, VA Medical Center/University of California San Diego, San Diego, CA
Background/Purpose: We have previously demonstrated that chondrocyte deficient in both TLR2 and TLR4 almost completely abolished pro-catabolic responses to rHMGB1 and LMW-HA, which are known…
Abstract Number: 2705 • 2015 ACR/ARHP Annual Meeting
AAA-Atpase p97-HDAC6 Controlled Poly-Ubiquitin Turnover Regulates Apoptotic and Autophagy-Associated Cell Death in Arthritis
Masaru Kato¹, Kerstin Klein², Caroline Ospelt², Christoph Kolling³, Michihito Kono¹, Shinsuke Yasuda¹, Renate E. Gay⁴, Steffen Gay⁵ and Tatsuya Atsumi¹, ¹Division of Rheumatology, Endocrinology and Nephrology, Hokkaido University Graduate School of Medicine, Sapporo, Japan, ²Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland, ³Schulthess Clinic, Zurich, Switzerland, ⁴Center of Experimental Rheumatology, University Hospital Zurich, Switzerland, Zurich, Switzerland, ⁵Center of Experimental Rheumatology, University Hospital Zurich, University Zurich, Zurich, Switzerland
Background/Purpose: The AAA-ATPase valosin containing protein (p97) and histone deacetylase 6 (HDAC6) interact with each other and are implicated in the degradation of ubiquitin-labelled proteins.…
Abstract Number: 2678 • 2014 ACR/ARHP Annual Meeting
UC-MSCs Inhibit T Cell Autophagy and Apoptosis in Patients with Systemic Lupus Erythematosus through Mitochondrial Transfer
Jinyun Chen¹, Xuebing Feng² and Lingyun Sun², ¹The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China, ²Department of Rheumatology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China
Background/Purpose This study is aimed to investigate the role of umbilical cord derived mesenchymal stem cells (UC-MSCs) on autophagy and apoptosis in T cells from…
Abstract Number: 1720 • 2014 ACR/ARHP Annual Meeting
GATA6 Deficiency Activates UPR Pathways in Endothelial Cells during the Development of Pulmonary Arterial Hypertension
Rong Han¹, Rosanne Van Deuren², Stefania Lenna¹, Izabela Chrobak¹, Timothy Radstake³, Carol Feghali-Bostwick⁴ and Maria Trojanowska¹, ¹Arthritis Center, Boston University, Boston, MA, ²Rheumatology Department, University Medical Center Nijmegen, Nijmegen, Netherlands, ³University Medical Center Utrecht, Utrecht, Netherlands, ⁴Medical University of South Carolina, Charleston, SC
Background/Purpose: Pulmonary arterial hypertension (PAH) is a severe lung complication of systemic sclerosis (SSc), and accounts for a large proportion of SSc-related deaths. As a…
Abstract Number: 1008 • 2014 ACR/ARHP Annual Meeting
Autophagy Activation Protects from Mitochondrial Dysfunction in Human Chondrocytes
Beatriz Carames¹, Paloma López de Figueroa², Martin Lotz³ and Francisco J. Blanco⁴, ¹Cartilage Biology Group. Rheumatology Division, INIBIC–A Coruña, SPAIN, A Coruña, Spain, ²Cartilage Biology group. Rheumatology Division, INIBIC-A Coruña, Spain, A Coruña, Spain, ³The Scripps Research Institute, La Jolla, USA, La Jolla, CA, ⁴Rheumatology Division, INIBIC-A Coruña, Spain, A Coruña, Spain
Background/Purpose Autophagy, is a key pathway of cellular homeostasis for removing damaged macromolecules and organelles, including mitochondria. Recent studies indicate that autophagy activation is defective…

All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].