Late‐in‐life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts

Protein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age‐associated cardiac dysfunction. Macroautophagy is the process by which post‐mitotic cells such as cardiomyocytes clear def...

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Bibliographic Details
Published in:Aging cell 2021-10, Vol.20 (10), p.e13467-n/a
Main Authors: Cho, Jae Min, Park, Seul‐Ki, Ghosh, Rajeshwary, Ly, Kellsey, Ramous, Caroline, Thompson, Lauren, Hansen, Michele, Mattera, Maria Sara de Lima Coutinho, Pires, Karla Maria, Ferhat, Maroua, Mookherjee, Sohom, Whitehead, Kevin J., Carter, Kandis, Buffolo, Márcio, Boudina, Sihem, Symons, J. David
Format: Article
Language:English
Subjects:
Adolescent
Adult
Age
Aged
Aged, 80 and over
Aging
Animals
Autophagy
Autophagy - physiology
Body composition
Cardiac function
Cardiomyocytes
Cardiomyopathy
Citrate synthase
Exercise
Fitness equipment
Fitness training programs
Heart - physiopathology
Heart diseases
Humans
Hypotheses
Male
Mice
Middle Aged
Muscle contraction
Organelles
Original Paper
Original Papers
Oxidative stress
Phagocytosis
Physical Conditioning, Animal - methods
Physical fitness
Physical training
protein aggregates
Protein Aggregates - physiology
Protein expression
Proteins
Quality control
Running
Soleus muscle
Young Adult
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Summary:Protein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age‐associated cardiac dysfunction. Macroautophagy is the process by which post‐mitotic cells such as cardiomyocytes clear defective proteins and organelles. We hypothesized that late‐in‐life exercise training improves autophagy, protein aggregate clearance, and function that is otherwise dysregulated in hearts from old vs. adult mice. As expected, 24‐month‐old male C57BL/6J mice (old) exhibited repressed autophagosome formation and protein aggregate accumulation in the heart, systolic and diastolic dysfunction, and reduced exercise capacity vs. 8‐month‐old (adult) mice (all p 
ISSN:1474-9718
1474-9726
DOI:10.1111/acel.13467