PM 2.5 Exposure Lowers Mitochondrial Endurance During Cardiac Recovery in a Rat Model of Myocardial Infarction.

Many studies have reported the negative effect of PM 2.5  exposure on heart function which is likely to impair postcardiac surgery rehabilitation that is involved in recovery and wound healing, yet the direct effects of PM 2.5  from diesel exhaust (DPM) on cardiac recovery is unknown. To study the impact of DPM on cardiac recovery and repair, we utilized isoproterenol induced myocardial infarction (MI) model where female rats were exposed to DPM prior and after MI induction. The experimental groups comprise of normal, ISO control, DPM control (42 days of exposure), DPM exposed prior (21 days) and after (21 days) MI induction (D + I + D) and DPM exposed (21 days) after MI (I + D). Post-MI rat hearts from D + I + D group exhibited higher fibrosis, elevated cardiac injury and altered electrophysiology, where this pathology was also observed in I + D group animals which was mild. Loss of mitochondrial quality was evident in DPM exposed animals with and without MI, where severe mitochondrial damage persisted in D + I + D group. In addition, these animals showed striking decline in ETC enzyme activity, ATP levels, mitochondrial copy number and down regulation of PGC1-α, TFAM and POLG along with the genes involved in mitophagy and mitofusion. Besides, the MI associated inactivation of cardio protective signalling pathways like PI3K and Akt were persistent in D + I + D group. In fact, I + D group animals also showed a similar pattern of change, but in a mild form. Taken together, exposure to PM 2.5  increases the risk, frequency or progression of MI by impairing the recovery potential of the myocardium.