David Hammers

David Hammers,

Assistant Professor

Department: MD-PHARMACOLOGY / THERAPEUTICS
Business Phone: (352) 273-9977
Business Email: dhammers@ufl.edu

Teaching Profile

Courses Taught
2020-2024
GMS6476 Fundamentals of Skeletal Muscle
2023
PAS5026 Pharmacotherapeu 2
2024
GMS6560 Molecules to Man: Past, Present and Future Therapeutic Strategies for Disease
2024
DEN6262 Prin of Pharmacology

Research Profile

The Hammers Lab researches physiological and pathophysiological mechanisms of skeletal and cardiac muscle, particularly those associated with genetic diseases known as muscular dystrophies. The primary motivation of these efforts is to identify potential therapeutic targets that can be exploited to develop treatments for muscle and heart diseases using small molecules and/or adeno-associated virus (AAV)-based gene therapies.

In recent work, the Hammers Lab has identified a group of repurposed drugs that act as “remodeling therapeutics” when used to treat severely diseased muscles by reducing muscle fibrosis and rejuvenating muscle regeneration. These discoveries have led to the initiation of new projects investigating the cellular dynamics that occur during the progression of muscle diseases in the absence and presence of remodeling therapeutics, as well as evaluating the potential for these remodeling therapeutics to improve the long-term efficacy of other current or emerging muscular dystrophy treatment strategies.

Areas of Interest
  • Cardiomyopathy
  • Fibrosis
  • Gene therapy
  • Muscular dystrophy
  • Regeneration
  • Striated Muscle Physiology
  • Therapeutic Development
Open Researcher and Contributor ID (ORCID)

0000-0003-2129-4047

Publications

2023
Blocking muscle wasting via deletion of the muscle-specific E3 ligase MuRF1 impedes pancreatic tumor growth.
Communications biology. 6(1) [DOI] 10.1038/s42003-023-04902-2. [PMID] 37179425.
2023
Blocking muscle wasting via deletion of the muscle-specific E3 ubiquitin ligase MuRF1 impedes pancreatic tumor growth.
Research square. [DOI] 10.21203/rs.3.rs-2524562/v1. [PMID] 36798266.
2023
Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration.
Nature communications. 14(1) [DOI] 10.1038/s41467-023-39506-1. [PMID] 37355632.
2023
Magnetic resonance quantification of skeletal muscle lipid infiltration in a humanized mouse model of Duchenne muscular dystrophy.
NMR in biomedicine. 36(3) [DOI] 10.1002/nbm.4869. [PMID] 36331178.
2022
Author response: The skeletal muscle circadian clock regulates titin splicing through RBM20
. [DOI] 10.7554/elife.76478.sa2.
2022
Evaluating Genetic Modifiers of Duchenne Muscular Dystrophy Disease Progression Using Modeling and MRI.
Neurology. 99(21):e2406-e2416 [DOI] 10.1212/WNL.0000000000201163. [PMID] 36240102.
2022
Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy
Journal of Molecular and Cellular Cardiology Plus. 1 [DOI] 10.1016/j.jmccpl.2022.100012. [PMID] 37206988.
2022
NOX4 inhibition promotes the remodeling of dystrophic muscle
JCI Insight. 7(20) [DOI] 10.1172/jci.insight.158316. [PMID] 36278481.
2022
The skeletal muscle circadian clock regulates titin splicing through RBM20
eLife. 11 [DOI] 10.7554/elife.76478.
2021
Author response: Filopodia powered by class x myosin promote fusion of mammalian myoblasts
. [DOI] 10.7554/elife.72419.sa2.
2021
Filopodia powered by class x myosin promote fusion of mammalian myoblasts
eLife. 10 [DOI] 10.7554/elife.72419.
2021
NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1
PLOS Genetics. 17(11) [DOI] 10.1371/journal.pgen.1009933. [PMID] 34807912.
2020
Glucocorticoids counteract hypertrophic effects of myostatin inhibition in dystrophic muscle
JCI Insight. 5(1) [DOI] 10.1172/jci.insight.133276. [PMID] 31830002.
2020
The D2.mdx mouse as a preclinical model of the skeletal muscle pathology associated with Duchenne muscular dystrophy.
Scientific reports. 10(1) [DOI] 10.1038/s41598-020-70987-y. [PMID] 32826942.
2019
Effects of PDE5 inhibition on dystrophic muscle following an acute bout of downhill running and endurance training.
Journal of applied physiology (Bethesda, Md. : 1985). 126(6):1737-1745 [DOI] 10.1152/japplphysiol.00664.2018. [PMID] 30946638.
2019
Functional muscle hypertrophy by increased insulin-like growth factor 1 does not require dysferlin.
Muscle & nerve. 60(4):464-473 [DOI] 10.1002/mus.26641. [PMID] 31323135.
2019
MYOD1 functions as a clock amplifier as well as a critical co-factor for downstream circadian gene expression in muscle.
eLife. 8 [DOI] 10.7554/eLife.43017. [PMID] 30789342.
2019
RevAMP(K)ing Mitochondria for Sarcoglycanopathy Therapeutics.
Circulation. Heart failure. 12(4) [DOI] 10.1161/CIRCHEARTFAILURE.119.005873. [PMID] 30922065.
2019
Smooth muscle atrophy and colon pathology in SMN deficient mice.
American journal of translational research. 11(3):1789-1799 [PMID] 30972202.
2018
Muscle Contraction.
Cold Spring Harbor perspectives in biology. 10(2) [DOI] 10.1101/cshperspect.a023200. [PMID] 29419405.
2018
The Nuclear Receptor PPARγ Controls Progressive Macrophage Polarization as a Ligand-Insensitive Epigenomic Ratchet of Transcriptional Memory.
Immunity. 49(4):615-626.e6 [DOI] 10.1016/j.immuni.2018.09.005. [PMID] 30332629.
2017
Supraphysiological levels of GDF 11 induce striated muscle atrophy
EMBO Molecular Medicine. 9(4):531-544 [DOI] 10.15252/emmm.201607231. [PMID] 28270449.
2016
Activin Receptor Type IIB Inhibition Improves Muscle Phenotype and Function in a Mouse Model of Spinal Muscular Atrophy.
PloS one. 11(11) [DOI] 10.1371/journal.pone.0166803. [PMID] 27870893.
2016
Increased collagen cross-linking is a signature of dystrophin-deficient muscle.
Muscle & nerve. 54(1):71-8 [DOI] 10.1002/mus.24998. [PMID] 26616495.
2016
Tadalafil Treatment Delays the Onset of Cardiomyopathy in Dystrophin-Deficient Hearts.
Journal of the American Heart Association. 5(8) [DOI] 10.1161/JAHA.116.003911. [PMID] 27506543.
2015
Anti-inflammatory macrophages improve skeletal muscle recovery from ischemia-reperfusion.
Journal of applied physiology (Bethesda, Md. : 1985). 118(8):1067-74 [DOI] 10.1152/japplphysiol.00313.2014. [PMID] 25678696.
2015
Controlled delivery of SDF-1α and IGF-1: CXCR4(+) cell recruitment and functional skeletal muscle recovery.
Biomaterials science. 3(11):1475-86 [DOI] 10.1039/c5bm00233h. [PMID] 26247892.
2012
Controlled release of IGF-I from a biodegradable matrix improves functional recovery of skeletal muscle from ischemia/reperfusion.
Biotechnology and bioengineering. 109(4):1051-9 [DOI] 10.1002/bit.24382. [PMID] 22095096.
2011
Impairment of IGF-I expression and anabolic signaling following ischemia/reperfusion in skeletal muscle of old mice.
Experimental gerontology. 46(4):265-72 [DOI] 10.1016/j.exger.2010.11.002. [PMID] 21094246.
2011
Ishemia-reperfusion enhances GAPDH nitration in aging skeletal muscle.
Aging. 3(10):1003-17 [PMID] 22027257.
2010
Functional assessment of skeletal muscle regeneration utilizing homologous extracellular matrix as scaffolding.
Tissue engineering. Part A. 16(4):1395-405 [DOI] 10.1089/ten.TEA.2009.0226. [PMID] 19929169.
2010
Repair of traumatic skeletal muscle injury with bone-marrow-derived mesenchymal stem cells seeded on extracellular matrix.
Tissue engineering. Part A. 16(9):2871-81 [DOI] 10.1089/ten.TEA.2009.0826. [PMID] 20412030.
2008
Functional deficits and insulin-like growth factor-I gene expression following tourniquet-induced injury of skeletal muscle in young and old rats.
Journal of applied physiology (Bethesda, Md. : 1985). 105(4):1274-81 [DOI] 10.1152/japplphysiol.90418.2008. [PMID] 18669936.

Contact Details

Phones:
Business:
(352) 273-9977
Emails:
Business:
dhammers@ufl.edu
Addresses:
Business Mailing:
PO Box 100267
GAINESVILLE FL 32610
Business Street:
ARB Building R5-234
1200 Newell Drive
GAINESVILLE FL 32610