Ross Summer, MD
Philadelphia, PA 19107
(215) 955-0830 fax
Research and Clinical Interests
Dr Summer's laboratory focuses on lung metabolism and understanding how local and systemic metabolic derangements contribute to the onset and progression of lung diseases.
One major area of investigation is on the relationship between obesity and acute lung injury. Recent epidemiological studies indicate that a paradoxical relationship exists between obesity and acute lung injury, in that, obese individuals are at increased risk for developing acute lung injury but outcomes in established disease are improved when compared to lean patients. In these investigations, Dr Summer's laboratory is utilizing genetic and diet-induced obesity models to understand how injury and inflammatory responses differ during obesity. These studies aim to direct future clinical investigations focusing on the prevention and the treatment of acute lung injury in lean and obese subjects.
In related studies, Dr Summer's laboratory is investigating the association between hormonal responses from adipose tissue and outcomes in acute lung injury. It is now increasingly apparent that adipose tissue is not just a storage depot for fuel but an important endocrine organ that secretes a multitude of hormones called adipokines. These adipokines act on virtually all tissues, including lung, and serve to regulate diverse biological processes involved in immune, metabolic and vascular regulation. Recent work from Dr Summer's laboratory has identified a relationship between plasma levels of the adipokine adiponectin and outcomes in patients with respiratory failure from diverse etiologies. In ongoing investigations, his laboratory will investigate whether a similar association exists in patients with respiratory failure from acute lung injury. Adiponectin oligomeric fractions will be measured in plasma samples obtained from patients participating in the National Heart, Lung and Blood Institute ARDS Network Fluid and Catheter Treatment Trial (FACTT). The goal of this study is determine whether measuring adiponectin oligomers is useful for predicting outcomes in patients with acute lung injury
Another major focus of Dr Summer's laboratory is on intermediary metabolism in the lung and understanding how alterations in local metabolic activity contribute to the progression of lung diseases. Our current hypothesis is that metabolic stress resulting from lung injury drives the inflammatory and the reparative responses seen in many pathological lung conditions (e.g. idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, acute lung injury). The goal of these studies is to identify novel therapeutic targets of metabolic pathways that can be used for treating lung diseases.
Most Recent Peer-Reviewed Publications
- Target-Specific Delivery of an Antibody That Blocks the Formation of Collagen Deposits in Skin and Lung
- Obesity-induced endoplasmic reticulum stress causes lung endothelial dysfunction and promotes acute lung injury
- T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity
- Therapeutic advances in idiopathic pulmonary fibrosis
- C1q deficiency promotes pulmonary vascular inflammation and enhances the susceptibility of the lung endothelium to injury
- Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury
- Direct effects of leptin and adiponectin on peripheral reproductive tissues: A critical review
- Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension
- IL-15Rα is a determinant of muscle fuel utilization, and its loss protects against obesity
- A pneumocyte-macrophage paracrine lipid axis drives the lung toward fibrosis
- Plasma adiponectin, clinical factors, and patient outcomes during the acute respiratory distress syndrome
- Pleiotropic effects of cavin-1 deficiency on lipid metabolism
- Extracellular ATP mediates the late phase of neutrophil recruitment to the lung in murine models of acute lung injury
- Chronic alcohol ingestion in rats alters lung metabolism, promotes lipid accumulation, and impairs alveolar macrophage functions
- Scleroderma-related lung disease: Are Adipokines Involved Pathogenically?
- Obesity paradox?
- Obesity: "Priming" the lung for injury
- MicroRNA-638 is highly expressed in human vascular smooth muscle cells and inhibits PDGF-BB-induced cell proliferation and migration through targeting orphan nuclear receptor NOR1
- Cavin1; a Regulator of Lung Function and Macrophage Phenotype
- The adipokine adiponectin has potent anti-fibrotic effects mediated via adenosine monophosphate-activated protein kinase: Novel target for fibrosis therapy