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Decreased production of adiponectin and/or elevated expression of A-FABP are important contributors to the pathogenesis of obesity-induced endothelial dysfunction and cardiovascular disease.
Sphingolipids and altered sphingolipid metabolism have emerged as potential key contributors to the pathogenesis of asthma.
Type III secreted effectors are major contributors to the pathogenesis of Salmonella infections.
Numerous reports indicate that oxidative stress and chronic inflammation are key contributors to the pathogenesis of atherosclerosis.
Multiple lines of evidence link pesticides as possible contributors to the pathogenesis of Parkinson's disease (PD).
BBBD and subsequent edema are major contributors to the pathogenesis of epilepsy.
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Inflammation is a central contributor to the pathogenesis of CF pulmonary disease.
It is known that gut dysbioses and atopobioses71 (colloquially referred to as 'leaky gut') are a well-known contributor to the pathogenesis of many metabolic diseases, including obesity146, T1D147, 148, T2D146, 149, 150, and CVD151.
Genetic susceptibility is an important contributor to the pathogenesis of Crohn's disease (CD).
Despite of these progresses, whether adiponectin deficiency is a direct contributor to the pathogenesis of breast cancer remain elusive.
Oxidative damage is believed to be an important contributor to the pathogenesis of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) [1].
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