Ryszard T. Smoleński

ORCID: 0000-0002-0190-9414
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About
Contact & Profiles
Research Areas
  • Adenosine and Purinergic Signaling
  • Cardiac Ischemia and Reperfusion
  • Mitochondrial Function and Pathology
  • Biochemical and Molecular Research
  • Transplantation: Methods and Outcomes
  • Adipose Tissue and Metabolism
  • Neonatal Health and Biochemistry
  • Cardiovascular Function and Risk Factors
  • Metabolism and Genetic Disorders
  • Pancreatic function and diabetes
  • PARP inhibition in cancer therapy
  • Organ Transplantation Techniques and Outcomes
  • Tissue Engineering and Regenerative Medicine
  • Xenotransplantation and immune response
  • Advanced MRI Techniques and Applications
  • Cardiac Arrest and Resuscitation
  • Diet and metabolism studies
  • Calcium signaling and nucleotide metabolism
  • Fuel Cells and Related Materials
  • Cancer, Hypoxia, and Metabolism
  • Heat shock proteins research
  • Mechanical Circulatory Support Devices
  • Cardiac Valve Diseases and Treatments
  • Nitric Oxide and Endothelin Effects
  • Metabolism, Diabetes, and Cancer

Gdańsk Medical University
2016-2025

Harefield Hospital
2004-2023

University of Milano-Bicocca
2013-2015

University of Cincinnati
2014

Environmental Protection Agency
2014

Imperial College London
2001-2011

Royal Brompton & Harefield NHS Foundation Trust
2006-2011

St James's University Hospital
2009

University Teaching Hospital
2009

University of Minnesota
2006

Although sepsis is the major cause of mortality and morbidity in critically ill, precise mechanism(s) causing multiorgan dysfunction remain unclear. Findings impaired oxygen utilization septic patients animals implicate nitric oxide-mediated inhibition mitochondrial respiratory chain. We recently reported a relationship between skeletal muscle dysfunction, clinical severity, poor outcome with shock. thus developed long-term, fluid-resuscitated, fecal peritonitis model utilizing male Wistar...

10.1152/ajpregu.00432.2003 article EN AJP Regulatory Integrative and Comparative Physiology 2004-02-04

Vascular endothelial growth factor (VEGF) is a promising reagent for inducing myocardial angiogenesis. Skeletal myoblast transplantation has been shown to improve cardiac function in chronic heart failure models by regenerating muscle. We hypothesized that of VEGF-expressing myoblasts could effectively treat acute infarction providing VEGF-induced cardioprotection through vasodilatation the early phase, followed angiogenesis effects salvaging ischemic host myocardium combined with functional...

10.1161/hc37t1.094524 article EN Circulation 2001-09-18

Interleukin-1 (IL-1) plays a role in mediating acute inflammation during ischemia-reperfusion (I/R) injury the heart, which leads to both necrosis and apoptosis of cardiomyocytes. IL-1 receptor antagonist (IL-1ra) is known inhibit effects IL-1alpha IL-1beta, resulting attenuated inflammatory injury, protect cells from IL-1beta-induced vitro. We hypothesized that IL-1ra overexpression would provide cardioprotection by reducing inflammation-mediated myocardial damage including after I/R...

10.1161/hc37t1.094871 article EN Circulation 2001-09-18

ABSTRACT Survival and proliferation of skeletal myoblasts within the cardiac environment are crucial to therapeutic efficacy myoblast transplantation heart. We have analyzed early dynamics implanted into myocardium investigated mechanisms underlying graft attrition. At 10 min after implantation [ 14 C]thymidine‐labeled male female mice hearts, C measurement showed that 39.2 ± 3.0% grafted cells survived, this steadily decreased 16.0 1.7% by 24 h 7.4 0.9% 72 h. PCR male‐ specific Smcy gene...

10.1096/fj.03-1308fje article EN The FASEB Journal 2004-05-20

Adult cardiac tissue undergoes a rapid process of dedifferentiation when cultured outside the body. The in vivo environment, particularly constant electromechanical stimulation, is fundamental to regulation structure and function. We investigated role stimulation preventing culture-induced adult using rat, rabbit human heart failure myocardial slices. Here we report that application preload equivalent sarcomere length (SL) = 2.2 μm optimal for maintenance rat slice structural, functional...

10.1038/s41467-019-10175-3 article EN cc-by Nature Communications 2019-05-15

Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) are effective substrates for NAD synthesis, which may act as vasoprotective agents. Here, we characterize the effects of NMN NR on endothelial inflammation dysfunction test involvement CD73 in these effects.The effect IL1β- or TNFα-induced (ICAM1 vWF expression), intracellular concentration NAD-related enzyme expression (NAMPT, CD38, CD73), were studied HAECs. The angiotensin II-induced impairment endothelium-dependent...

10.1016/j.bcp.2020.114019 article EN cc-by-nc-nd Biochemical Pharmacology 2020-05-08

Upregulation of heat shock protein 70 (HSP70) is beneficial in cardioprotection against ischemia-reperfusion injury, but the mechanism action unclear. We studied role HSP70 overexpression through gene therapy on mitochondrial function and ventricular recovery a protocol that mimics clinical donor heart preservation.Hemagglutinating virus Japan (HVJ)-liposome technique was used to transfect isolated rat hearts via intracoronary infusion either (HSP group, n=16) or no (CON n=16), which...

10.1161/hc37t1.094932 article EN Circulation 2001-09-18

Heat shock protein 72 (HSP72) is known to provide myocardial protection against ischemia-reperfusion injury by its chaperoning function. Target molecules of this effect are presumed include not only structural proteins but also other self-preservation proteins. The details, however, remain unknown. Manganese superoxide dismutase (Mn-SOD) an enzyme that preserves mitochondria, a key organelle for cellular respiration, from reperfusion and limits mitochondria-related apoptosis. We hypothesized...

10.1161/01.cir.0000032880.55215.92 article EN Circulation 2002-09-24

Graft survival after skeletal myoblast transplantation is affected by various pathological processes caused environmental stress. Heat shock known to afford protection of several aspects cell metabolism and function. We hypothesized that prior heat treatment graft cells would improve their transplantation.L6 rat myoblasts expressing ss-galactosidase (ss-gal) were subjected (42 degrees C, 1 hour). Increased expression protein 72 was detected 24 hours later in the heat-shocked cells. After...

10.1161/01.cir.102.suppl_3.iii-216 article EN Circulation 2000-11-07

Reservoirs are a globally significant source of methane (CH4), although most measurements have been made in tropical and boreal systems draining undeveloped watersheds. To assess the magnitude CH4 emissions from reservoirs midlatitude agricultural regions, we measured carbon dioxide (CO2) emission rates William H. Harsha Lake (Ohio, U.S.A.), an impacted reservoir, over 13 month period. The reservoir was strong throughout year, emitting on average 176 ± 36 mg C m(-2) d(-1), highest profile...

10.1021/es501871g article EN publisher-specific-oa Environmental Science & Technology 2014-08-26

Toll-like receptors (TLRs) are the central players in innate immunity. In particular, TLR9 initiates inflammatory response by recognizing DNA, imported infection or released from tissue damage. Inflammation is, however, harmful to terminally differentiated organs, such as heart and brain, with poor regenerative capacity, yet role of nonimmune cells, including cardiomyocytes neurons, is undefined. Here we uncover an unexpected energy metabolism cellular protection neurons. stimulation reduced...

10.1073/pnas.1219243110 article EN Proceedings of the National Academy of Sciences 2013-03-11

Huntington's disease (HD) is a fatal neurodegenerative disorder, caused by polyglutamine expansion in the huntingtin protein (HTT). HD has peripheral component to its pathology: skeletal muscles are severely affected, leading atrophy and malfunction both pre-clinical clinical settings. We previously used two symptomatic mouse models demonstrate impairment of contractile characteristics hind limb muscles, which was accompanied significant loss function motor units. The mice displayed...

10.3389/fphys.2017.00127 article EN cc-by Frontiers in Physiology 2017-03-02

Skeletal myoblast transplantation is promising for the treatment of end-stage heart failure. Direct intramyocardial injection useful local cell delivery but may not be effective in global dissemination cells into heart, which would advantageous treating generalized cardiac dysfunction as dilated cardiomyopathy. We hypothesized that intracoronary infusion myoblasts disseminate more effectively, leading to functional improvement failure.Heart failure was induced by intraperitoneal...

10.1161/hc37t1.094929 article EN Circulation 2001-09-18

ABSTRACT Ischemia‐reperfusion injury, a clinical problem during cardiac surgery, involves worsened adenosine trisphosphate (ATP) generation and damage to the heart. We studied carbon monoxide (CO) pretreatment, proven valuable in rodents but not previously tested large animals, for its effects on pig hearts subjected cardiopulmonary bypass with cardioplegic arrest. Hearts of CO‐treated pigs showed significantly higher ATP phosphocreatine levels, less interstitial edema, apoptosis...

10.1096/fj.03-0996fje article EN The FASEB Journal 2004-05-07

Background— Combination therapy consisting of mechanical unloading using a left ventricular assist device (LVAD) and pharmacological intervention can promote recovery from end-stage heart failure, but the mechanism is unknown. Preliminary microarray analysis revealed significant unexpected decrease in myocardial arginine:glycine amidinotransferase (AGAT) gene expression during these patients. The aim this study was to evaluate role AGAT failure recovery. Methods Results— We used quantitative...

10.1161/circulationaha.105.000448 article EN Circulation 2006-07-04

After myocardial infarction (MI), adverse remodeling with left ventricular (LV) dilatation is a major determinant of poor outcome. Skeletal myoblast (SkM) implantation improves cardiac function post-MI, although the mechanism unclear. IL-1 influences post-MI hypertrophy and collagen turnover implicated in SkM death after grafting. We hypothesized that expressing secretory receptor antagonist (sIL-1ra) at MI border zones would specifically attenuate exhibit improved graft cell number. Stable...

10.1073/pnas.0306205101 article EN Proceedings of the National Academy of Sciences 2004-03-12
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