Eric J. Gonzalez
Duke University
13 Papers
11 Citations
Eric J. Gonzalez is an academic researcher from Duke University. The author has contributed to research in topics: Urinary bladder & Urinary system. The author has an hindex of 7, co-authored 13 publications. Previous affiliations of Eric J. Gonzalez include Durham University & University of Vermont.
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Papers
The Role(s) of Cytokines/Chemokines in Urinary Bladder Inflammation and Dysfunction
TL;DR: In this paper, the authors describe chemokine/receptor (CXCL12/CXCR4; CCL2/CCR2) signaling and cytokine/Receptor (transforming growth factor (TGF-β)/TGFβ type 1 receptor) signaling that may be valuable LUT targets for pharmacologic therapy to improve urinary bladder function and reduce somatic sensitivity associated with urinary bladder inflammation.
The Effects of Tempol on Cyclophosphamide-Induced Oxidative Stress in Rat Micturition Reflexes
Eric J. Gonzalez,Abbey Peterson,Susan E. Malley,Mitchel Daniel,Daniel Lambert,Michael Kosofsky,Margaret A. Vizzard +6 more
TL;DR: It is demonstrated that reducing oxidative stress in CYP-induced cystitis improves urinary bladder function and reduces markers of oxidative stress and inflammation.
Bladder sensory physiology: neuroactive compounds and receptors, sensory transducers, and target-derived growth factors as targets to improve function
TL;DR: This work reviews studies related to the organization of the afferent limb of the micturition reflex and discusses neuroplasticity in an animal model of urinary bladder inflammation to increase the understanding of functional bladder disorders and to identify potential novel targets for development of therapeutic interventions.
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Expression and function of transforming growth factor-β isoforms and cognate receptors in the rat urinary bladder following cyclophosphamide-induced cystitis
TL;DR: Evidence is provided for the involvement of TGF-β in lower urinary tract neuroplasticity following urinary bladder inflammation, a functional role of T GF-β signaling in the afferent limb of the micturition reflex, and urinary bladder TβR-1 as a viable target to reduce voiding frequency with cystitis.
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Purinergic signalling underlies transforming growth factor-β-mediated bladder afferent nerve hyperexcitability.
TL;DR: A causal link between an inflammatory mediator, TGF‐β, and intrinsic signalling mechanisms of the urothelium that may contribute to the altered sensory processing of bladder filling is established.
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