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Protein Carbonylation as a Mechanistic Driver and Biomarker of Sarcopenia

Award Number: K99AG101344
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 09/11/2026
PERIOD OF PERFORMANCE END DATE: 08/31/2028

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Protein Carbonylation as a Mechanistic Driver and Biomarker of Sarcopenia - ABSTRACT By 2050 the number of individuals over the age of 80y will triple to reach 426 million. Unfortunately, the rate of age-related comorbidities has also increased precipitously as our global population has continued to age. Currently, there is no clinically approved treatment for age-related functional decline creating demand for the development of such treatments. Carbonyls are reactive electrophilic metabolites that accumulate in contexts of increased oxidative stress, such as aging. This carbonyl stress damages macromolecules such as proteins, lipids, and DNA. Our lab demonstrated that carbonyl stress is exacerbated in muscles during a hindlimb unloading (HU) model of inactivity. Importantly, the accumulation of proteins modified by the reactive lipid carbonyl 4HNE, as well as muscle dysfunction and atrophy, were attenuated in HU mice treated with the carbonyl-scavenging dipeptide N-acetyl-carnosine (N-Ac-Carn). Therefore, we hypothesize that N-Ac-Carn could prevent carbonyl stress in aging muscle. Our preliminary data demonstrates preserved muscle function in 24-month-old male and female mice that had been treated with N-Ac-Carn over six months compared to control. The current proposed project will test the efficacy of genetically overexpressing the lipid-hydroperoxide detoxing enzyme GPx4 and N-Ac-Carn treatment to attenuate muscle decline with age. I also aim to elucidate the mechanisms by which carbonyl stress impairs muscle function during aging by using a novel mass spectrometry method to comprehensively characterize the carbonyl proteomes in muscle with age. N-Ac-Carn is an endogenously produced dipeptide that is safe for human consumption and affordable making it a promising therapeutic strategy for the mitigation of age-related functional decline. In addition, our novel proteomics approach will uncover which carbonylation events on proteins are most relevant to manifestations of features of sarcopenia in mice and in humans.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $144,053 )
2026	2026	UNIVERSITY OF UTAH	201 PRESIDENTS CIR	SALT LAKE CITY	UT	84112	SALT LAKE	USA	Aging Research	000	1	9/11/2026	NEW	$144,053
														Subtotal = $144,053

Grand Total All Awards = $144,053

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Protein Carbonylation as a Mechanistic Driver and Biomarker of Sarcopenia

Award Number: K99AG101344

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 09/11/2026

PERIOD OF PERFORMANCE END DATE: 08/31/2028

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