Study links polymer-specific nanoplastic exposure to mitochondrial dysfunction and depressed cardiac ejection fraction in humans

A study in Cardiovascular Research reports that circulating polystyrene and polyethylene nanoplastics are associated with reduced left ventricular ejection fraction in older adults, driven by polymer-specific mitochondrial stress and impaired quality-control pathways.

Researchers quantified circulating levels of polystyrene (PS) and polyethylene (PE) in older adults without major comorbidities and measured left ventricular ejection fraction (EF) using transthoracic echocardiography.

Circulating levels of both PS and PE were significantly higher in participants with EF <50% compared to those with EF ≥50% (PE p=0.021; PS p<0.001), with PS remaining independently associated with depressed EF after multivariable adjustment.

In vitro exposure of human AC16 cardiomyocytes to PS nanoplastics resulted in a loss of respiratory capacity, reduced spare respiratory capacity, and suppressed basal and maximal respiration.

PE exposure in vitro caused a distinct compensatory remodeling pattern characterized by reduced maximal respiration but increased ATP-linked respiration and tighter respiratory coupling.

Proteomic profiling of exposed cardiomyocytes revealed a mitochondria-centered injury signature, including the disruption of mitochondrial protein import, altered redox buffering, and incomplete activation of mitochondrial quality-control pathways.

This study establishes a direct link between polymer-specific environmental nanoplastic exposure and clinical cardiac impairment in older human populations.

The identification of polymer-specific toxic mechanisms helps explain how different environmental contaminants selectively impair myocardial bioenergetics.

The discovery that nanoplastic-induced cardiomyocyte injury is accompanied by an incomplete activation of mitochondrial quality-control pathways suggests that restoring these pathways could mitigate cardiotoxic damage.

These findings emphasize the potential clinical utility of therapeutic platforms designed to protect mitochondrial health and enhance cellular resilience against environmental pollutants.

The study may stimulate investment and research into pipelines focused on restoring mitochondrial respiration and metabolic flexibility in cardiac tissues.

Future clinical studies validating these findings in larger, diverse cohorts and investigating the efficacy of mitochondrial-targeted agents in protecting cardiomyocytes from nanoplastic-induced injury.