Steven Jeffrey Sollott MD
Cardiologist | Cardiovascular Disease
5600 Nathan Shock Dr Gerontology Research Baltimore MD, 21224Rating
5/5
About
Dr. Steven Sollott is a cardiologist practicing in Baltimore, MD. Dr. Sollott specializes in diagnosing, monitoring, and treating diseases or conditions of the heart and blood vessels and the cardiovascular system. These conditions include heart attacks, heart murmurs, coronary heart disease, and hypertension. Dr. Sollott also practices preventative medicine, helping patients maintain a heart-healthy life.
Education and Training
Univ of Rochester Sch of Med & Dentistry, Rochester Ny 1984
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Cardiovascular Disease
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Activation of distinct cAMP-dependent and cGMP-dependent pathways by nitric oxide in cardiac myocytes.
- Glucagon-like peptide-1 does not mediate amylase release from AR42J cells.
- Reactive oxygen species (ROS)-induced ROS release: a new phenomenon accompanying induction of the mitochondrial permeability transition in cardiac myocytes.
- The old heart: operating on the edge.
- Glucagon-like peptide-1 increases cAMP but fails to augment contraction in adult rat cardiac myocytes.
- Endogenous nitric oxide mechanisms mediate the stretch dependence of Ca2+ release in cardiomyocytes.
- Perspectives on mammalian cardiovascular aging: humans to molecules.
- Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153. Ca2+ increases transcriptional activity and mRNA stability.
- The "heartbreak" of older age.
- Glycogen synthase kinase-3beta mediates convergence of protection signaling to
- Examining intracellular organelle function using fluorescent probes: from animalcules to quantum dots.
- Protection in the aged heart: preventing the heart-break of old age?
- Mitochondrial ROS-induced ROS release: an update and review.
- Hexokinase II detachment from mitochondria triggers apoptosis through the permeability transition pore independent of voltage-dependent anion channels.
- The identity and regulation of the mitochondrial permeability transition pore: where the known meets the unknown.
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