Jordan Fuqua, Ph.D.

Office: 329 O’Donoghue Research Building
Lab: 325 O’Donoghue Research Building

• Ph.D. Human Physiology, University of Iowa, Iowa City, Iowa  2020
• M.S. Exercise Physiology, Brigham Young University, Provo, Utah  2015
• B.S. Exercise Science, Brigham Young University, Provo, Utah  2013

• American Physiological Society 

Sarcopenia is the progressive loss of skeletal muscle mass and function with age, and is a major driver of frailty, loss of independence, and poor recovery from illness or injury in older adults. My research focuses on understanding how aging and periods of disuse, such as bedrest during hospitalization, accelerate muscle decline. I also study why recovery of muscle function is often incomplete in older individuals following disuse atrophy. These problems have profound consequences on healthspan and quality of life, yet there are still no effective therapies to maintain or restore muscle function. Through my work, I aim to develop strategies that can preserve muscle strength and promote recovery, with the long-term goal of extending independence and improving quality of life in older adults. 

Through my research program I aim to identify the underlying mechanisms that lead to impaired skeletal muscle maintenance with aging and limited recovery after disuse. I focus on proteostatic mechanisms such as protein synthesis and degradation, which are critical regulators of skeletal muscle mass and function. Particularly, I study the autophagy-lysosome pathway, transcription factor EB (TFEB), mTOR, and lysosomal function as interconnected regulators of proteostasis and as key mechanisms supporting skeletal muscle maintenance and recovery during aging.

Skeletal muscle maintenance is highly responsive to nutrient availability and metabolic state, which regulate mTOR, TFEB, and the autophagy-lysosome pathway to coordinate protein turnover and organelle quality control. Defining how these nutrient-sensing mechanisms preserve muscle quality will provide critical insight into mechanisms of healthy aging and identify opportunities for therapeutic intervention. My research leverages dietary interventions, including calorie restriction and fasting, to determine how modulation of these pathways can preserve muscle function, mitigate sarcopenia, and enhance recovery following disuse.

• National Istitutes of Health, Investigating TFEB as a critical node to improve proteostatic maintenance and skeletal muscle function with age, K99/R00. Principle investigator, 2024-2029, $1,017,000 

NCBI bibliography

• Gimla M, Olszewski S, Brown JL, Raymond-Pope C, Rigsby S, Peelor III FF, Hae Ryong K, Yao L, Olson LE, Fuqua JD, Miller BF. Overactive PDGFRα and PDGFRβ promote distinct yet overlapping phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving drastic muscle growth. AJP Cell, 2026 Apr, PMID: 41509204
• Mesquita PHC, Halle JL, Fuqua JD, Miller BF. Applying lessons from limb muscle disuse and ageing to better understand ventilator-induced diaphragm dysfunction. Exp Physiol, 2025 Jul, PMID: 40638619
• Fuqua JD, Mesquita PHC, Taylor ME, Borowik AK. Muscle-specific mitophagy: insights into hindlimb and diaphragm responses during health and sepsis. J Physiol, 2024 Oct, PMID: 39222396
• Musci RV, Fuqua JD, Peelor FF, Nguyen HVM, Richardson A, Choi S, Miller BF, Wanagat J. Age-induced changes in skeletal muscle mitochondrial DNA synthesis, quantity, and quality in genetically unique rats. Geroscience, 2024 Sep, PMID: 39312152
• Fuqua JD, Lawrence MM, Hettinger Z, Borowik AK, Brecheen PL, Szczygiel MM, Abbott CB, Peelor FF, Confides AL, Kinter M, Bodine SC, Dupont-Versteegden EE, Miller BF. Impaired Proteostatic Mechanisms Other Than Decreased Protein Synthesis, Limits Old Skeletal Muscle Recovery After Disuse Atrophy. JCSM, 2023 July, PMCID: PMC10570113
• Penniman CM, Bhardwaj G, Nowers CJ, Brown CU, Junck TL, Boyer CK, Jena J, Fuqua JD, Lira VA, O'Neill BT. Loss of FoxOs in muscle increases strength and mitochondrial function during aging. J Cachexia Sarcopenia Muscle. 2022 Nov, PMID: 36442857 
• Harris MP, Zhang QJ, Cochran CT, Ponce J, Alexander S, Kronemberger A, Fuqua JD, Zhang Y, Fattal R, Harper T, Murry ML, Grueter CE, Abel ED, Lira VA. Perinatal versus adult loss of ULK1 and ULK2 distinctly influences cardiac autophagy and function. Autophagy. 2022 Feb, PMCID: PMC9466614 
• Lamin V, Verry J, Eigner-Bybee I, Fuqua JD, Wong T, Lira VA, Dokun AO. Modulation of miR-29a and ADAM12 reduces post-ischemic skeletal muscle injury and improves perfusion recovery and skeletal muscle function in a mouse model of type 2 diabetes and peripheral artery disease. Int J Mol Sci. 2022 Jan, PMCID: PMC8745107 
• Sousa LGO, Marshall AG, Norman JE, Fuqua JD, Lira VA, Rutledge JC, Bodine SC. The effects of diet composition and chronic obesity on muscle growth and function. J Appl Physiol, 2021 Jan, PMCID: PMC7944928
• Bhardwaj G, Penniman CM, Jena J, Suarez Beltran PA, Foster C, Poro K, Junck TL, Hinton AO Jr, Souvenir R, Fuqua JD, Morales PE, Bravo-Sagua R, Sivitz WI, Lira VA, Abel ED, O'Neill BT. Insulin and IGF-1 receptors regulate complex-I dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle. J Clin Invest. 2021 Aug, PMID: 34343133.
• Fuqua JD, Mere CP, Kronemberger A, Blomme J, Bae D, Turner KD, Harris MP, Scudese E, Edwards M, Ebert SM, Sousa LGO, Bodine SC, Yang L, Adams CM, Lira VA. ULK2 is essential for degradation of ubiquitinated protein aggregates and homeostasis in skeletal muscle. FASEB J, 2019 Aug, PMCID: PMC6902739   
• Ramos AM, Senna GW, Scudese E, Dantas EHM, Silva-Grigoletto ME, Fuqua JD, and Pardono E. Cardiovascular and strength adaptations in concurrent training in hypertensive women. Revista Brasileira de Medicina do Esporte 25, no. 5 (2019): 367-371. 
• Sorensen JR, Fuqua JD, Dehyle MR, Parmley J, Skousen C, Hancock C, Parcell AC, Hyldahl RD. Preclinical characterization of the JAK/STAT inhibitor SGI-1252 on skeletal muscle function, morphology, and satellite cell content. PLoS One, 2018 June, PMCID: PMC5999283.