Tim Lahm

ORCID: 0000-0003-0007-6606
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About
Contact & Profiles
Research Areas
  • Pulmonary Hypertension Research and Treatments
  • Cardiovascular Function and Risk Factors
  • Cardiovascular Issues in Pregnancy
  • Neonatal Respiratory Health Research
  • Cardiovascular and exercise physiology
  • Cardiovascular Effects of Exercise
  • Congenital Heart Disease Studies
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Apelin-related biomedical research
  • Heart Failure Treatment and Management
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Nitric Oxide and Endothelin Effects
  • High Altitude and Hypoxia
  • Respiratory Support and Mechanisms
  • Mesenchymal stem cell research
  • Eicosanoids and Hypertension Pharmacology
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Cardiac Ischemia and Reperfusion
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Cardiac Arrest and Resuscitation
  • Hormonal Regulation and Hypertension
  • Renin-Angiotensin System Studies
  • Cancer, Hypoxia, and Metabolism
  • Venous Thromboembolism Diagnosis and Management
  • Liver Disease and Transplantation

National Jewish Health
2021-2025

University of Colorado Denver
2021-2025

University of Colorado Anschutz Medical Campus
2022-2025

Denver School of Nursing
2025

The Medical Center of Aurora
2025

Veterans Health Administration
2023-2025

Indiana University
2012-2024

Richard L. Roudebush VA Medical Center
2014-2023

Canadian Respiratory Research Network
2023

Indiana University School of Medicine
2013-2022

Understanding the mechanisms by which adult stem cells produce growth factors may represent an important way to optimize their beneficial paracrine and autocrine effects. Components of wound milieu stimulate factor production promote cell-mediated repair. We hypothesized that tumor necrosis factor-α (TNF-α), endotoxin (LPS), or hypoxia activate human mesenchymal (MSCs) increase release vascular endothelial (VEGF), fibroblast 2 (FGF2), insulin-like 1 (IGF-1), hepatocyte (HGF) nuclear...

10.1152/ajpcell.00437.2007 article EN AJP Cell Physiology 2008-01-31

Background— Pulmonary hypertension (PH) is associated with increased morbidity across the cardiopulmonary disease spectrum. Based primarily on expert consensus opinion, PH defined by a mean pulmonary artery pressure (mPAP) ≥25 mm Hg. Although mPAP levels below this threshold are common among populations at risk for PH, relevance of <25 Hg to clinical outcome unknown. Methods and Results— We analyzed retrospectively all US veterans undergoing right heart catheterization (2007–2012) in...

10.1161/circulationaha.115.020207 article EN Circulation 2016-02-13

Pregnancy outcomes in patients with pulmonary hypertension remain poor despite advanced therapies. Although consensus guidelines recommend against pregnancy hypertension, it may nonetheless occasionally occur. This guideline document sought to discuss the state of knowledge effects on vascular disease and define usual practice avoidance management. is based systematic review peer-reviewed, published literature identified MEDLINE. The strength was graded, when inadequate support high-level...

10.1086/682230 article EN Pulmonary Circulation 2015-07-08

Rationale: 17β-Estradiol (E2) attenuates hypoxic pulmonary vasoconstriction and hypertension (HPH) through an unknown mechanism that may involve estrogen receptors (ER) or E2 conversion to catecholestradiols methoxyestradiols with previously unrecognized effects on cardiopulmonary vascular remodeling.Objectives: To determine the by which exerts protective in HPH.Methods: Male rats were exposed hypobaric hypoxia while treated (75 μg/kg/d) vehicle. Subgroups cotreated pharmacologic...

10.1164/rccm.201107-1293oc article EN American Journal of Respiratory and Critical Care Medicine 2012-03-03

Bone marrow mesenchymal stem cells (MSCs) may be a novel treatment modality for organ ischemia, possibly through the release of beneficial paracrine factors. However, an age threshold likely exists as to when MSCs gain their protective properties. We hypothesized that 1) VEGF would crucial cell mediator in providing postischemic myocardial protection and 2) small-interfering (si)RNA ablation adult (aMSCs) equalize differences observed between aMSC- neonatal (nMSC)-mediated cardioprotection....

10.1152/ajpheart.00565.2008 article EN AJP Heart and Circulatory Physiology 2008-10-11

Estrogens are disease modifiers in PAH. Even though female patients exhibit better right ventricular (RV) function than men, estrogen effects on RV (a major determinant of survival PAH) incompletely characterized. We sought to determine whether sex differences exist the SuHx model PAH, hormone depletion females worsens function, and E2 repletion improves adaptation. Furthermore, we studied contribution ERs mediating E2's effects. SuHx-induced pulmonary hypertension (SuHx-PH) was induced male...

10.1152/ajplung.00006.2015 article EN AJP Lung Cellular and Molecular Physiology 2015-02-26

ABSTRACT Fibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed following puberty pregnancy. We previously demonstrated that the combination iron deficiency and a knock-in R176Q FGF23 mutation in mature mice induced expression hypophosphatemia paralleled late-onset ADHR phenotype. Because anemia pregnancy premature infants is common, goal this study was test whether alters phosphate...

10.1002/jbmr.2049 article EN Journal of Bone and Mineral Research 2013-07-22

Women with pulmonary arterial hypertension (PAH) exhibit better right ventricular (RV) function and survival than men; however, the underlying mechanisms are unknown. We hypothesized that 17β-estradiol (E2), through estrogen receptor α (ER-α), attenuates PAH-induced RV failure (RVF) by upregulating procontractile prosurvival peptide apelin via a BMPR2-dependent mechanism. found ER-α expression were decreased in homogenates from patients RVF rats maladaptive (but not adaptive) remodeling....

10.1172/jci129433 article EN Journal of Clinical Investigation 2021-01-26

17β-Estradiol (E 2 ) exerts protective effects on right ventricular (RV) function in pulmonary arterial hypertension (PAH). Since acute exercise-induced increases afterload may lead to RV dysfunction PAH, we sought determine whether E allows for superior adaptation after an exercise challenge. We studied echocardiographic, hemodynamic, structural, and biochemical markers of male female rats with sugen/hypoxia (SuHx)-induced hypertension, as well ovariectomized (OVX) SuHx females, or without...

10.1152/ajplung.00132.2016 article EN AJP Lung Cellular and Molecular Physiology 2016-06-11

Exercise is beneficial in pulmonary arterial hypertension (PAH), although studies to date indicate little effect on the elevated pressures or maladaptive right ventricle (RV) hypertrophy associated with disease. For chronic left failure, high-intensity interval training (HIIT) promotes greater endothelial stimulation and superior benefit than customary continuous exercise (CExT); however, HIIT has not been tested for PAH. Therefore, here we investigated acute responses vs. CExT a rat model...

10.1152/ajpregu.00358.2016 article EN AJP Regulatory Integrative and Comparative Physiology 2016-10-26

Rationale: Pulmonary arterial hypertension (PAH) is characterized by structural remodeling of pulmonary arteries and arterioles. Underlying biological processes are likely reflected in a perturbation circulating proteins. Objectives: To quantify analyze the plasma proteome patients with PAH using inherited genetic variation to inform on underlying molecular drivers. Methods: An aptamer-based assay was used measure proteins 357 idiopathic or heritable PAH, 103 healthy volunteers, 23 relatives...

10.1164/rccm.202109-2106oc article EN American Journal of Respiratory and Critical Care Medicine 2022-04-08

Rationale: Genetic studies suggest that SOX17 (SRY-related HMG-box 17) deficiency increases pulmonary arterial hypertension (PAH) risk. Objectives: On the basis of pathological roles estrogen and HIF2α (hypoxia-inducible factor 2α) signaling in artery endothelial cells (PAECs), we hypothesized is a target promotes mitochondrial function attenuates PAH development via inhibition. Methods: We used metabolic (Seahorse) promoter luciferase assays PAECs together with chronic hypoxia murine model...

10.1164/rccm.202203-0450oc article EN cc-by-nc-nd American Journal of Respiratory and Critical Care Medicine 2023-03-13
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