Smooth muscle cells from patients with asthma have increased numbers of mitochondria (arrows).

In patients with asthma, airway smooth muscle cells make too many mitochondria, say Trian et al. on page 3173. Instead of easing breathing, these mitochondrial masses trigger cell division, leading to a choking build-up of smooth muscle cells.

Many chronic lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD), are characterized by an increased mass of smooth muscle in the bronchi, which causes the airways to constrict. Although bronchial dilators ease acute asthma attacks, they have no effect on the muscle build-up.

In patients with asthma, these muscle cells were known to divide excessively, but what prompted this cell division was unclear. Trian et al. now show that an overdose of calcium influx triggers the expression of mitochondria-building transcription factors in the cells.

The resulting construction of new mitochondria—and subsequent burst in ATP production—gave the cells the energy boost needed for proliferation. This pathway was specific to patients with asthma, as mitochondria numbers and activity were not increased in cells from patients with COPD. Smooth muscle cell proliferation in COPD patients, by contrast, was driven by anaerobic glycolysis.

Calcium channel blockers, which have been shown to relieve asthma attacks and block tumor cell proliferation, might thus also reverse the smooth muscle cell accumulation that perpetuates chronic disease.