Friedrich Luft (medical doctor)

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Friedrich C. Luft (born March 4, 1942 in Berlin ) is an American physician ( nephrologist ). He is known for research on high blood pressure .

Life

Luft is the son of the altitude physiologist Ulrich Cameron Luft and the nephew of the well-known Berlin theater critic Friedrich Luft . He grew up in the USA from 1947, where he studied zoology at Colorado College (bachelor's degree in 1964) and medicine at Thomas Jefferson University with a doctorate (MD) in 1968. He spent two years in the US Army . From 1975 to 1989 he was a professor in the department of renal medicine ( nephrology ) and intensive care medicine at the Indiana University School of Medicine in Indianapolis , with a full professorship from 1982. In the USA he was admitted as a specialist in internal medicine, nephrology and intensive care medicine. From 1984 to 1986 he was a visiting scholar at Heidelberg University . In 1989 he became a professor at the University of Erlangen-Nuremberg and in 1992 he became head of the department of nephrology, genetics and high blood pressure at the Franz Volhard Clinic for Cardiovascular Diseases of the Charité in Berlin-Buch, and then in 2001 at the Helios Clinic Berlin -Book, he was head of internal medicine and nephrology. In 2010 he resigned from his clinical functions.

Since it was founded in 2007, he has been director of the Experimental and Clinical Research Center (ECRC) in Berlin-Buch by Charité and the Max Delbrück Center for Molecular Medicine (MDC) in Berlin-Buch, which is part of the Helmholtz Society . He has headed a research group at the MDC since 1992.

He has also been the Helen C. Levitt Visiting Professor at the University of Iowa (Roy J. and Lucille A. Carver College of Medicine) since 2007 .

He is a US citizen.

plant

In the 2010s he and his colleagues achieved a breakthrough in high blood pressure research, which resulted from decades of genetic testing (from 1994) of a Turkish family from Anatolia. Half of the family members suffered from extreme (on average 50 mmHg above a normal value of 140/90 mmHg) genetically caused high blood pressure, which, if left untreated, usually led to death before the age of 50. At the same time, those affected had shortened fingers ( brachydactyly type E). The researchers were able to narrow down the cause of the hereditary disease to point mutations in the PDE3A gene on chromosome 12 , which codes for the enzyme phosphodiesterase-3a . The enzyme breaks down the important secondary messenger substance cAMP and the genetic defect led to the overexpression of phosphodiesterase 3a and increased cAMP breakdown. On the one hand, this means that the smooth muscle cells in the blood vessel walls divide more intensely and the vessel walls become thicker (high blood pressure); on the other hand, it affects the expression of the PTHLH gene ( parathyroid hormone like hormone) in cartilage cells, which is responsible for cartilage growth It is important: cAMP deficiency means that it cannot be read out (brachydactyly). The high blood pressure mechanism discovered by Luft and his colleagues works only through the blood vessels and not through the kidneys. This rare autosomal dominant hereditary disease is now called Bilginturan syndrome after the endocrinologist Ahmet Nihat Bilginturan .

Air also examined the salt sensitivity of the human body and influences on, for example, genetic type (like a certain haptoglobin - phenotype ). In 1983, Luft and colleagues showed that there was no connection between the rate of saline excretion via the kidneys (for example, after high salt consumption) and high blood pressure. Later, however, he and his colleagues discovered another mechanism in the body's salt balance that creates high blood pressure. In rats, they succeeded in discovering a previously unknown storage mechanism for table salt in the skin, the disruption of which causes high blood pressure. The salt is stored in the interstitium between the cells, caused by the stimulation of the formation of lymph vessels via the growth factor VEGF-C (vascular endothelial growth factor C), which is controlled by macrophages .

With his research group, he developed a method to use magnetic resonance imaging to map the distribution of saline in the body.

Further research by Luft and his colleagues concerns vascular inflammation and its genetic causes.

Honors and memberships

Web links

References and comments

  1. First described in 1973 by Nihat Bilginturan from the University of Haceteppe in Ankara. The publication was brought to air by the geneticist Thomas Wienker .
  2. Philipp G. Maass, Atakan Aydin, Friedrich C. Luft, Carolin Schächterle, Okan Toka, Sylvia Bähring and others. a .: PDE3A mutations cause autosomal dominant hypertension with brachydactyly . In: Nature Genetics , Volume 47, 2015, pp. 647-653, abstract
  3. Barbara Bachtler: MDC and Charité researchers identify the gene that triggers high blood pressure and short fingers . MDC, May 2015
  4. ^ MH Weinberger, JZ Miller, FC Luft, CE Grim, NS Fineberg: Definitions and characteristics of sodium sensitivity and blood pressure resistance . In: Hypertension , Volume 8, Supl. II, 1986, pp. II-127-II-134
  5. ^ MH Weinberger, JZ Miller, NS Fineberg, FC Luft, CE Grim, JC Christian: Association of haptoglobin with sodium sensitivity and resistance of blood pressure . In: Hypertension , Volume 10, 1987, pp. 443-446, abstract
  6. ^ F. Luft, LI Rankin, L. Bloch, LR Willis, NS Fineberg, MH Weinberger: The effects of rapid saline infusion on sodium excretion, renal function, and blood pressure at different sodium intakes in man . In: American Journal of Kidney Disease , Volume 2, 1983, pp. 464-470, PMID 6823962 .
  7. Agnes Machnik, Dominik N. Müller, Wolfgang Derer, Friedrich Luft, Jens Titze a. a .: Macrophages regulate salt-dependent volume and blood pressure by a vascular endothelial growth factor-C-dependent buffering mechanism . In: Nature Medicine , Vol. 15, 2009, pp. 545-552, PMID 19412173 .
  8. Member entry by Prof. Dr. Friedrich C. Luft (with picture) at the German Academy of Sciences Leopoldina , accessed on February 18, 2016.