Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease

Ignazio Grattagliano, Liliana P. Montezinho, Paulo J. Oliveira, Gema Frühbeck, Javier Gómez-Ambrosi, Fabrizio Montecucco, Federico Carbone, Mariusz R. Wieckowski, David Q.H. Wang, Piero Portincasa

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by the excessive accumulation of triglycerides in hepatocytes. NAFLD is the most frequent chronic liver disease in developed countries, and is often associated with metabolic disorders such as obesity and type 2 diabetes. NAFLD definition encompasses a spectrum of chronic liver abnormalities, ranging from simple steatosis (NAFL), to steatohepatitis (NASH), significant liver fibrosis, cirrhosis, and hepatocellular carcinoma. NAFLD, therefore, represents a global public health issue. Mitochondrial dysfunction occurs in NAFLD, and contributes to the progression to the necro-inflammatory and fibrotic form (NASH). Disrupted mitochondrial function is associated with a decrease in the energy levels and impaired redox balance, and negatively affects cell survival by altering overall metabolism and subcellular trafficking. Such events reduce the tolerance of hepatocytes towards damaging hits, and favour the injurious effects of extra-cellular factors. Here, we discuss the role of mitochondria in NAFLD and focus on potential therapeutic approaches aimed at preserving mitochondrial function.

Original languageEnglish (US)
Pages (from-to)34-45
Number of pages12
JournalBiochemical Pharmacology
Volume160
DOIs
StatePublished - Feb 1 2019

Fingerprint

Mitochondria
Liver
Fatty Liver
Liver Cirrhosis
Hepatocytes
Developed Countries
Type 2 Diabetes Mellitus
Oxidation-Reduction
Non-alcoholic Fatty Liver Disease
Liver Diseases
Hepatocellular Carcinoma
Cell Survival
Triglycerides
Chronic Disease
Public Health
Obesity
Public health
Medical problems
Metabolism
Electron energy levels

Keywords

  • Fatty liver
  • Mitochondria
  • Nitrosative stress
  • Nonalcoholic fatty liver disease
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology

Cite this

Grattagliano, I., Montezinho, L. P., Oliveira, P. J., Frühbeck, G., Gómez-Ambrosi, J., Montecucco, F., ... Portincasa, P. (2019). Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease. Biochemical Pharmacology, 160, 34-45. https://doi.org/10.1016/j.bcp.2018.11.020

Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease. / Grattagliano, Ignazio; Montezinho, Liliana P.; Oliveira, Paulo J.; Frühbeck, Gema; Gómez-Ambrosi, Javier; Montecucco, Fabrizio; Carbone, Federico; Wieckowski, Mariusz R.; Wang, David Q.H.; Portincasa, Piero.

In: Biochemical Pharmacology, Vol. 160, 01.02.2019, p. 34-45.

Research output: Contribution to journalReview article

Grattagliano, I, Montezinho, LP, Oliveira, PJ, Frühbeck, G, Gómez-Ambrosi, J, Montecucco, F, Carbone, F, Wieckowski, MR, Wang, DQH & Portincasa, P 2019, 'Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease' Biochemical Pharmacology, vol. 160, pp. 34-45. https://doi.org/10.1016/j.bcp.2018.11.020
Grattagliano I, Montezinho LP, Oliveira PJ, Frühbeck G, Gómez-Ambrosi J, Montecucco F et al. Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease. Biochemical Pharmacology. 2019 Feb 1;160:34-45. https://doi.org/10.1016/j.bcp.2018.11.020
Grattagliano, Ignazio ; Montezinho, Liliana P. ; Oliveira, Paulo J. ; Frühbeck, Gema ; Gómez-Ambrosi, Javier ; Montecucco, Fabrizio ; Carbone, Federico ; Wieckowski, Mariusz R. ; Wang, David Q.H. ; Portincasa, Piero. / Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease. In: Biochemical Pharmacology. 2019 ; Vol. 160. pp. 34-45.
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