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ABSTRACT: Effect of aircraft anti-icer on soil metatranscriptome

PROVIDER: PRJNA738857 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14848917_1.fastq.gz	Fastqsanger.gz
	SRR14848917_2.fastq.gz	Fastqsanger.gz
	SRR14848918_1.fastq.gz	Fastqsanger.gz
	SRR14848918_2.fastq.gz	Fastqsanger.gz
	SRR14848919_1.fastq.gz	Fastqsanger.gz

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Project description:Environmental stressors present in the modern world can have a fundamental effect on the physiology and health of humans. Exposure to stressors like air pollution, heat and traffic noise has been linked to a pronounced increase in non-communicable diseases. Specifically, aircraft noise has been identified as a risk factor for cardiovascular and metabolic diseases, such as arteriosclerosis, heart failure, stroke and diabetes. Noise stress leads to neuronal activation with subsequent stress hormone release that ultimately leads to activation of the renin-angiotensin-aldosterone system, increasing inflammation and oxidative stress, with dramatic effects on the cardiovascular system. However, despite the epidemiological evidence of a link between noise stress and metabolic dysfunction, the consequences of exposure at the molecular, metabolic level of the cardiovascular system are largely unknown. Here we use a murine model system of aircraft noise exposure to show that noise stress profoundly alters heart metabolism. Within days of exposing animals to aircraft noise the heart has a reduced potential for utilising fatty-acid beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain for generating ATP. This is compensated by shifting energy production towards glycolysis. Intriguingly, the metabolic shift is reminiscent of what is observed in failing and ischaemic hearts. Our results demonstrate that within a relatively short exposure time, the cardiovascular system undergoes a fundamental metabolic shift that bears the hallmarks of cardiovascular disease. Overall, aircraft noise induces rapid, detrimental metabolic shifts in the heart, resembling patterns seen in cardiovascular diseases. These findings underscore the urgent need to comprehend molecular consequences of environmental stressors, paving the way for targeted interventions aiming mitigating health risks associated with chronic noise exposure in our modern, noisy environments.

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