Carbamazepine alone and in combination with doxycycline attenuates isoproterenol-induced cardiac hypertrophy.

β-adrenergic signaling is involved in the development of cardiac hypertrophy (CH), justifying the use of β-blockers as a therapy to minimize and postpone the consequences of this disease. Evidence suggests that adenylate cyclase, a downstream effector of the β-adrenergic pathway, might be a therapeutic target. We examined the effects of the anti-epileptic drug carbamazepine (CBZ), an inhibitor of adenylate cyclase.

Doxycycline attenuates isoproterenol- and transverse aortic banding-induced cardiac hypertrophy in mice.

The United States Food and Drug Administration-approved antibiotic doxycycline (DOX) inhibits matrix metalloproteases, which contribute to the development of cardiac hypertrophy (CH). We hypothesized that DOX might serve as a treatment for CH. The efficacy of DOX was tested in two mouse models of CH: induced by the beta-adrenergic agonist isoproterenol (ISO) and induced by transverse aortic banding.