NNT deficiency alters cardiac structure and function without impairing mitochondrial bioenergetics in aged mice.

ABSTRACT: Proton-translocating NAD(P)⁺ transhydrogenase (NNT) is highly expressed in cardiac tissue, where it physiologically supports mitochondrial NADPH production. However, under certain pathological conditions, NNT may shift toward consuming the mitochondrial NADPH pool. Although NNT has been implicated in redox homeostasis, its contribution to cardiac function during aging remains uncertain. In this study, we assessed cardiac morphology and function, as well as mitochondrial bioenergetics and Ca²⁺ handling, in NNT-deficient (Nnt^-/-) mice and congenic wild-type controls (Nnt^+/+) at adult (5 months), middle (12 months), and older (23 months) ages. NNT-deficient mice developed age-related cardiac hypertrophy, along with a moderately reduced ejection frac

SUBMITTER: Dalla Costa AP 

PROVIDER: S-EPMC12681527 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature