Author
Manal F. Abdelmalek
Other affiliations: Indiana University, Mayo Clinic, Durham University ...read more
Bio: Manal F. Abdelmalek is an academic researcher from Duke University. The author has contributed to research in topics: Nonalcoholic fatty liver disease & Fatty liver. The author has an hindex of 59, co-authored 170 publications receiving 13482 citations. Previous affiliations of Manal F. Abdelmalek include Indiana University & Mayo Clinic.
Papers published on a yearly basis
Papers
More filters
••
Saint Louis University1, University of California, San Diego2, Virginia Commonwealth University3, Columbia University4, Johns Hopkins University5, Duke University6, Indiana University – Purdue University Indianapolis7, Case Western Reserve University8, University of California, San Francisco9, Virginia Mason Medical Center10, Cleveland Clinic11, Washington University in St. Louis12, National Institutes of Health13
TL;DR: Obeticholic acid improved the histological features of non-alcoholic steatohepatitis, but its long-term benefits and safety need further clarification.
1,798 citations
••
Pierre-and-Marie-Curie University1, French Institute of Health and Medical Research2, San Antonio Military Medical Center3, University of Antwerp4, Paris Diderot University5, Catholic University of Leuven6, University of Melbourne7, University of Angers8, Duke University9, University of Virginia10, Radboud University Nijmegen11, Newcastle University12, university of lille13, Virginia Commonwealth University14, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico15, Semmelweis University16
TL;DR: A post-hoc analysis of data from trial of patients with NASH showed that elafibranor (120 mg/d for 1 year) resolved NASH without fibrosis worsening, based on a modified definition, in the intention-to-treat analysis and in patients with moderate or severe NASH.
813 citations
••
TL;DR: The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption, and fructose resulted in dose-dependent increase in KHK protein and activity.
763 citations
••
TL;DR: In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis, a readily modifiable environmental risk factor that may ameliorate disease progression in patients withNAFLD.
622 citations
••
TL;DR: Small, more definitive trials are suggested to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.
537 citations
Cited by
More filters
••
TL;DR: A detailed understanding of epidemiologic factors and molecular mechanisms associated with HCC ultimately could improve current concepts for screening and treatment of this disease.
4,768 citations
••
TL;DR: Nonalcoholic fatty liver disease is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as due to cirrhosis and hepatocellular carcinoma, which occurs in a minority of patients.
Abstract: Nonalcoholic fatty liver disease (NAFLD) is present in up to one third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn, exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as due to cirrhosis and hepatocellular carcinoma, which occurs in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with 'cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.
4,705 citations
••
TL;DR: This guidance provides a data-supported approach to the diagnostic, therapeutic, and preventive aspects of NAFLD care.
4,431 citations
••
TL;DR: There are no systems for grading necroinflammatory activity or for staging fibrosis as exist for various other forms of chronic liver disease and this study proposes a grading and staging system that reflects the unique histological features of nonalcoholic steatohepatitis.
3,553 citations
••
TL;DR: Current understanding of the cellular and molecular mechanisms of fibrogenesis is explored and components of the renin–angiotensin–aldosterone system (ANG II) have been identified as important regulators of fibrosis and are being investigated as potential targets of antifibrotic drugs.
Abstract: Fibrosis is defined by the overgrowth, hardening, and/or scarring of various tissues and is attributed to excess deposition of extracellular matrix components including collagen. Fibrosis is the end result of chronic inflammatory reactions induced by a variety of stimuli including persistent infections, autoimmune reactions, allergic responses, chemical insults, radiation, and tissue injury. Although current treatments for fibrotic diseases such as idiopathic pulmonary fibrosis, liver cirrhosis, systemic sclerosis, progressive kidney disease, and cardiovascular fibrosis typically target the inflammatory response, there is accumulating evidence that the mechanisms driving fibrogenesis are distinct from those regulating inflammation. In fact, some studies have suggested that ongoing inflammation is needed to reverse established and progressive fibrosis. The key cellular mediator of fibrosis is the myofibroblast, which when activated serves as the primary collagen-producing cell. Myofibroblasts are generated from a variety of sources including resident mesenchymal cells, epithelial and endothelial cells in processes termed epithelial/endothelial-mesenchymal (EMT/EndMT) transition, as well as from circulating fibroblast-like cells called fibrocytes that are derived from bone-marrow stem cells. Myofibroblasts are activated by a variety of mechanisms, including paracrine signals derived from lymphocytes and macrophages, autocrine factors secreted by myofibroblasts, and pathogen-associated molecular patterns (PAMPS) produced by pathogenic organisms that interact with pattern recognition receptors (i.e. TLRs) on fibroblasts. Cytokines (IL-13, IL-21, TGF-beta1), chemokines (MCP-1, MIP-1beta), angiogenic factors (VEGF), growth factors (PDGF), peroxisome proliferator-activated receptors (PPARs), acute phase proteins (SAP), caspases, and components of the renin-angiotensin-aldosterone system (ANG II) have been identified as important regulators of fibrosis and are being investigated as potential targets of antifibrotic drugs. This review explores our current understanding of the cellular and molecular mechanisms of fibrogenesis.
3,390 citations