Fanconi anemia (FA) has been investigated since early studies based on two definitions, namely defective DNA repair and proinflammatory condition. The former definition has built up the grounds for FA diagnosis as excess sensitivity of patients’ cells to xenobiotics as diepoxybutane and mitomycin C, resulting in typical chromosomal abnormalities. Another line of studies has related FA phenotype to a prooxidant state, as detected by both in vitro and ex vivo studies. The discovery that the FA group G (FANCG) protein is found in mitochondria (Mukhopadhyay et al., 2006) has been followed by an extensive line of studies providing evidence for multiple links between other FA gene products and mitochondrial dysfunction. The fact that FA proteins are encoded by nuclear, not mitochondrial DNA does not prevent these proteins to hamper mitochondrial function, as it is recognized that most mitochondrial proteins are of nuclear origin. This body of evidence supporting a central role of mitochondrial dysfunction, along with redox imbalance in FA, should lead to the re-definition of FA as a mitochondrial disease.
Background: The population of older adults (ie, those aged ≥55 years) in England is becoming increasingly ethnically diverse.
Pulmonary arterial hypertension (PAH) occurs in women more than men whereas survival in men is worse than in women.
Background: Ambient air pollution is a major environmental cause of morbidity and mortality worldwide. Cities are generally hotspots for air pollution and disease.
The COVID-19 pandemic has stalled and rolled back progress on Sustainable Development Goals (SDGs).
Alzheimer's disease (AD) is the foremost cause of dementia among other neurodegenerative diseases, leading to memory loss and cognitive deficits.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain that ultimately results in the death of neurons and dementia.
Introduction: Skin diseases have a significant global impact on quality of life, mental health, and loss of income.
