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A Novel Mechanism of Autophagic Degradation in Cellular Senescence

Award Number: F32AG099362
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/20/2026
PERIOD OF PERFORMANCE END DATE: 08/19/2027

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A Novel Mechanism of Autophagic Degradation in Cellular Senescence - Project Summary Cellular senescence is characterized by stable cell cycle arrest and pro-inflammatory responses, contributing to both aging and disease. Autophagy is a self-digestion process, which maintains cellular homeostasis and is upregulated in senescence. The specific roles of autophagy in senescence remain poorly understood. The degradation of autophagy substrates requires ATG8 family proteins, which bind to substrates via protein-protein interactions. My preliminary data suggest that a specific ATG8 family protein can covalently conjugate to autophagy substrates in senescent cells, which facilitates protein autophagic degradation. Furthermore, this covalent conjugation-mediated autophagic degradation occurs specifically in senescence, and not in quiescence or starvation. I performed unbiased proteomic identification of covalently conjugated autophagy adaptor proteins in senescence, revealing numerous targets, including a demethylase. I plan to test the central hypothesis that covalent conjugation to autophagy adaptors represents a novel mechanism for degrading autophagy substrates in senescence, and propose that targeting this mechanism holds promise in intervening senescence-associated diseases. Specifically, in Aim 1, I propose to investigate the mechanisms of covalent conjugation in senescence, examining the key differences underlying senescence and starvation. In Aim 2, I propose to investigate the covalently conjugated demethylase identified from proteomics, focusing on its role in regulating key aspects of senescence. I further plan to actively engage in a variety of training and career development opportunities to facilitate my career progression. Overall, this project investigates a novel mechanism of substrate recognition by autophagy, and will shed new light on the biology of senescence. These findings could provide new insights into age-related diseases and potential therapeutic strategies for targeting senescent cells. The planned career and training activities will prepare me to become a future independent investigator.


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 = $79,510 )
2026	2026	THE GENERAL HOSPITAL CORPORATION	55 FRUIT ST	BOSTON	MA	02114	SUFFOLK	USA	Aging Research	001	1	4/1/2026	NEW	$1,260
2026	2026	THE GENERAL HOSPITAL CORPORATION	55 FRUIT ST	BOSTON	MA	02114	SUFFOLK	USA	Aging Research	000	1	2/20/2026	NEW	$78,250
														Subtotal = $79,510

Grand Total All Awards = $79,510

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A Novel Mechanism of Autophagic Degradation in Cellular Senescence

Award Number: F32AG099362

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/20/2026

PERIOD OF PERFORMANCE END DATE: 08/19/2027

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