FABP5 Deficiency Impairs Mitochondrial Function and Aggravates Pathological Cardiac Remodeling and Dysfunction.

Area of Science:

• Cardiology
• Molecular Biology
• Biochemistry

Background:

• Fatty acid-binding protein 5 (FABP5) is crucial for fatty acid metabolism.
• Its role in pathological cardiac remodeling and heart failure remains understudied.

Purpose of the Study:

• To investigate the role of FABP5 in transverse aortic constriction (TAC)-induced cardiac remodeling and dysfunction in mice.

Main Methods:

• Utilized quantitative RT-PCR, western blotting, echocardiography, histopathology, and transmission electron microscopy.
• Assessed mitochondrial function, oxidative stress, and myofibroblast activation in FABP5 knockout and wild-type mice, and in primary cardiac fibroblasts with FABP5 knockdown.

Main Results:

• FABP5 expression was upregulated in TAC-induced heart failure models.
• FABP5 deficiency exacerbated cardiac hypertrophy, fibrosis, and dysfunction post-TAC.
• FABP5 deficiency led to severe mitochondrial impairment and increased oxidative stress in cardiac tissues.

Conclusions:

• FABP5 deficiency aggravates pathological cardiac remodeling and dysfunction.
• This exacerbation is mediated by impaired cardiac mitochondrial function and increased oxidative stress.