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Carlos J. Pirola
University of Buenos Aires
163Publications
41H-index
5,379Citations
Publications 163
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Nonalcoholic steatohepatitis (NASH)—the severe histological form of nonalcoholic fatty liver disease (NAFLD)—is regarded as a major health problem worldwide (1,2). The disease can progress to liver cirrhosis and eventually to hepatocellular carcinoma (1,3). Treatment of NASH and NASH-fibrosis is thus increasingly being given priority in the clinical field.
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#1Silvia Sookoian (UBA: University of Buenos Aires)H-Index: 37
#2Carlos J. Pirola (UBA: University of Buenos Aires)H-Index: 41
Here, the authors review the remarkable genetic discoveries that have illuminated the biology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). The authors integrate genes associated with NAFLD and NASH into regulatory pathways to elucidate the disease pathogenesis. They review the evidence for molecular mediators of chronic liver damage, which suggests that convergent pathophenotypes, including inflammation and fibrosis, share common genetic modifiers. They fu...
1 CitationsSource
1 CitationsSource
#1Silvia Sookoian (UBA: University of Buenos Aires)H-Index: 37
#2Marco Arrese (UC: Pontifical Catholic University of Chile)H-Index: 36
Last.Carlos J. Pirola (UBA: University of Buenos Aires)H-Index: 41
view all 3 authors...
1 CitationsSource
Nonalcoholic fatty liver disease (NAFLD) is regarded as the most frequent cause of chronic liver damage (1,2). The natural history of the disease presents a complex scenario of potential progression into severe clinical outcomes, including nonalcoholic steatohepatitis (NASH), NASH-fibrosis, cirrhosis, and hepatocellular carcinoma (1,2). In addition, NAFLD is closely associated with comorbidities of the metabolic syndrome (MetS), including type 2 diabetes, obesity, arterial hypertension, and dysl...
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#1Silvia Sookoian (UBA: University of Buenos Aires)H-Index: 37
#2Diego Flichman (CONICET: National Scientific and Technical Research Council)H-Index: 2
Last.Carlos J. Pirola (UBA: University of Buenos Aires)H-Index: 41
view all 7 authors...
Current knowledge on the genetic basis of nonalcoholic fatty liver disease (NAFLD) suggests that variants contributing not only to the disease predisposition but histological severity as well are located in genes that regulate lipid metabolism. We explored the role of rs641738 C/T located in TMC4 (transmembrane channel-like 4) exon 1 (p.Gly17Glu) and 500 bases- downstream of MBOAT7 gene (TMC4/MBOAT7), in the genetic risk for developing NAFLD in a case-control study. Our sample included 634 indiv...
4 CitationsSource
#1Ludmila S. Peres Diaz (UBA: University of Buenos Aires)H-Index: 1
#2Mariano L. Schuman (UBA: University of Buenos Aires)H-Index: 8
Last.Silvia I. García (UBA: University of Buenos Aires)H-Index: 19
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Abstract Cardiac tyhrotropin-releasing hormone (TRH) is overexpressed in the hypertrophied left ventricle (LV) of spontaneously hypertensive rats (SHR) and its inhibition prevents both hypertrophy and fibrosis. In a normal heart, the TRH increase induces fibrosis and hypertrophy opening the question of whether TRH could be a common mediator of left ventricular hypertrophy (LVH). We used angiotensin II (AngII) as an inductor of LVH to evaluate if the blockade of LV-TRH prevents hypertrophy and fi...
2 CitationsSource
8 CitationsSource
#1Silvia Sookoian (UBA: University of Buenos Aires)H-Index: 37
#2Carlos J. Pirola (UBA: University of Buenos Aires)H-Index: 41
Abstract Phenotypic modulation of NAFLD-severity by molecules derived from white (adipokines) and brown (batokines) adipose tissue may be important in inducing or protecting against the progression of the disease. Adipose tissue-derived factors can promote the progression of NAFLD towards severe histological stages (NASH-fibrosis and NASHcirrhosis). This effect can be modulated by the release of adipokines or batokines that directly trigger an inflammatory response in the liver tissue or indirec...
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#1Mariana L. Tellechea (UBA: University of Buenos Aires)H-Index: 8
#2Melisa F. Mensegue (UBA: University of Buenos Aires)H-Index: 1
Last.Carlos J. Pirola (UBA: University of Buenos Aires)H-Index: 41
view all 3 authors...
Numerous rodent studies have evaluated the effects of a maternal high-fat diet (HFD) on later in life susceptibility to Metabolic Syndrome (MetS) with varying results. Our aim was to quantitatively synthesize the available data on effects of maternal HFD around gestation on offspring’s body mass, body fat, plasma leptin, glucose, insulin, lipids and systolic blood pressure (SBP). Literature was screened and summary estimates of the effect of maternal HFD on outcomes were calculated by using fixe...
11 CitationsSource
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