On 2016 Mar 18, Kaikobad Irani commented:

This valuable piece of work illustrates that skeletal muscle SIRT3 is a vital component of the metabolic program activated by inorganic nitrite which promotes glucose disposal in a rat model of metabolic syndrome/HFpEF. As such, it adds to the growing body of evidence that SIRT3 promotes insulin signaling in skeletal muscle.

However, the conclusion in the title that SIRT3 activation by nitrite normalizes pulmonary hypertension associated with HFpEF should be interpreted with caution. The data presented in this regard show correlation, not causation, as acknowledged in the Discussion. Causality demands proof that lack of SIRT3 exacerbates pulmonary hypertension, or activation of SIRT3 ameliorates it, in a suitable model of HFpEF.

On 2016 Mar 18, Kaikobad Irani commented:

This valuable piece of work illustrates that skeletal muscle SIRT3 is a vital component of the metabolic program activated by inorganic nitrite which promotes glucose disposal in a rat model of metabolic syndrome/HFpEF. As such, it adds to the growing body of evidence that SIRT3 promotes insulin signaling in skeletal muscle.

However, the conclusion in the title that SIRT3 activation by nitrite normalizes pulmonary hypertension associated with HFpEF should be interpreted with caution. The data presented in this regard show correlation, not causation, as acknowledged in the Discussion. Causality demands proof that lack of SIRT3 exacerbates pulmonary hypertension, or activation of SIRT3 ameliorates it, in a suitable model of HFpEF.