Sentence examples for mitochondrial deficiency from inspiring English sources

Compelling evidence implicates mitochondrial deficiency, oxidative stress, and inflammation as important pathogenic factors in PD.

The robust effects of CR on yeast mitochondrial mutants led us to pose the question: Are the beneficial effects of CR in the setting of mitochondrial deficiency conserved in mammals?

However, these arguments do not apply to a new version of the mitochondrial deficiency hypothesis proposed by Ritov et al. [12].

To examine whether the reduced ATP content in rpS6P−/− muscle may result from mitochondrial deficiency, we measured the activity of citrate synthase that is commonly used as an assessment of mitochondrial content [23].

As an organelle participating in cell signaling [27], we hypothesized that the mitochondrial deficiency reported herein could alter the production of signaling agents involved in the regulation of myogenic differentiation.

The mechanism by which "mitochondrial deficiency" is thought to cause insulin resistance is accumulation of intramuscular lipids as a result of a decreased capacity for fat oxidation [2], [9].

Mitochondrial deficiencies, and alterations in melanin granule number and distribution dominated the defects seen in PE.

We hypothesized that the overexpression of Tfam could inhibit mitochondrial deficiencies as well as left ventricular (LV) remodeling and failure in mice after myocardial infarction (MI).

This has prompted keen interest in the development of relevant cellular and animal models and in exploring innovative therapeutic strategies to modulate the mitochondrial deficiencies observed in these diseases.

Understanding the relationship between metabolic and mitochondrial deficiencies and the mechanisms underlying the pathology of MADD, in particular the neurological phenotypes, has been hampered by the rarity of the disorder and thus analyses of autopsy and other tissues has been limited[5].

Identification of mutations in SDH genes led to the first and unexpected demonstration of a tumor suppressor role for a metabolic enzyme (for review see [11], [12]), implicating mitochondrial deficiencies in tumorigenesis, as first suggested by Otto Warburg 80 years earlier.