Gary Desir

Last updated
Gary Desir
Born
Gary V. Desir
Alma mater New York University
Yale University
Known forDiscovery of Renalase
Spouses Deborah Dyett Desir [1] [2]
Scientific career
FieldsNephrology and molecular physiology
Institutions Yale University
Yale School of Medicine
VA Connecticut Healthcare System
School of Forestry and Environmental Studies
Albert Schweitzer Hospital

Gary V. Desir is a physician, researcher and medical practitioner who was appointed as the vice provost for faculty development and diversity at Yale University in March 2020. [3] [4] [5] Desir is also the chair of the department of internal medicine at Yale School of Medicine, and was formerly the chair of the Yale Medicine Board. His areas of specialization include nephrology and molecular physiology, the latter specifically about potassium channels. [6] His notable research work includes discovery of the kidney protein renalase. [7] [8] [9]

Contents

Early life and career

Desir was born in Haiti [10] and has studied rhétorique from St Louis de Gonzague. He moved to the US in 1972 and in 1973 he enrolled in the bachelors program at New York University. In 1976, he graduated as a BS in biology while receiving the membership of Phi Beta Kappa. [11] In 1980, he graduated with honors from Yale University and became part of the Alpha Omega Alpha. [12] From 1980 to 1983 he trained in internal medicine. He took part in the fellowship program in nephrology. He worked for 3 years as the research fellowship at Yale University in nephrology with specialization in potassium channels (molecular physiology).

In 1988, Desir was appointed as an assistant professor at Yale School of Medicine. He became associate professor and professor in 1993 and 2003 respectively. From 1997 to 2004, he served as the section chief of nephrology at the VA Connecticut Healthcare System. He worked as the chair of internal medicine at VACHS from 2004 to 2013. [13] In 2013, he was appointed on interim basis as the chair of the department of internal medicine at Yale School of Medicine. [14] He was appointed to the permanent chair in 2015. [15] In 2016 Desir was designated as the Paul B. Beeson Professor of Internal Medicine at Yale. [16] Desir is also vice provost for faculty development and diversity. [17] [18]

Research activities

Desir's most notable research activity include the discovery of the agent renalase, which is basically a renal protein. It can be classified as an enzyme as well as a hormone - such nature being decided on its site of action with the prospect of being used in dual-purpose. [19] The primary function of renalase is as an intracellular enzyme that controls and manipulates energy production at granular level. It also has the protective characteristics that it exhibits against cell injury and stress, once it secretes in the plasma. [20] [21]

Desir is also the founder of biotech firm Personal Therapeutics, that works exploring the prospects of commercializing renalase and its pathway while basing the foundations in two concepts, viz. renalase agonist and renalase antagonist. Renalase agonist primarily deals with the role of renalase in mitigating tissue injury in myocardial infarction whereas renalase antagonist is based on the concept of fighting cancer cells [22] which "highjack the renalase pathway as a survival mechanism". [23] [24] [25] During covid-19 pandemic, a correlation was claimed in a Yale researchers report between low levels of the renalase and poor outcome of clinical treatment of covid patients. [26] [27]

Other activities

Desir is an active advocate of diversity, equity and inclusion [28] and a founding member of the Minority Organization for Retention & Expansion executive committee of Yale. [29] [30] Under dual teaching appointment, Desir conducts the graduate course "Sustainable Development in a Post-Disaster Context" at the School of Forestry and Environmental Studies, in collaboration with the Albert Schweitzer Hospital in Deschapelles, Haiti. [31]

Notable publications

Related Research Articles

<span class="mw-page-title-main">Kidney dialysis</span> Removal of nitrogenous waste and toxins from the body in place of or to augment the kidney

Kidney dialysis is the process of removing excess water, solutes, and toxins from the blood in people whose kidneys can no longer perform these functions naturally. This is referred to as renal replacement therapy. The first successful dialysis was performed in 1943.

<span class="mw-page-title-main">Kidney disease</span> Damage to or disease of a kidney

Kidney disease, or renal disease, technically referred to as nephropathy, is damage to or disease of a kidney. Nephritis is an inflammatory kidney disease and has several types according to the location of the inflammation. Inflammation can be diagnosed by blood tests. Nephrosis is non-inflammatory kidney disease. Nephritis and nephrosis can give rise to nephritic syndrome and nephrotic syndrome respectively. Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.

<span class="mw-page-title-main">Hyperkalemia</span> Medical condition with excess potassium

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. Because necrosis is often not present, the term acute tubular injury (ATI) is preferred by pathologists over the older name acute tubular necrosis (ATN). ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. Common causes of ATN include low blood pressure and use of nephrotoxic drugs. The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN. Management relies on aggressive treatment of the factors that precipitated ATN. Because the tubular cells continually replace themselves, the overall prognosis for ATN is quite good if the underlying cause is corrected, and recovery is likely within 7 to 21 days.

<span class="mw-page-title-main">4-Aminopyridine</span> Chemical compound

4-Aminopyridine (4-AP, fampridine, dalfampridine) is an organic compound with the chemical formula C5H4N–NH2. The molecule is one of the three isomeric amines of pyridine. It is used as a research tool in characterizing subtypes of the potassium channel. It has also been used as a drug, to manage some of the symptoms of multiple sclerosis, and is indicated for symptomatic improvement of walking in adults with several variations of the disease. It was undergoing Phase III clinical trials as of 2008, and the U.S. Food and Drug Administration (FDA) approved the compound on January 22, 2010. Fampridine is also marketed as Ampyra (pronounced "am-PEER-ah," according to the maker's website) in the United States by Acorda Therapeutics and as Fampyra in the European Union, Canada, and Australia. In Canada, the medication has been approved for use by Health Canada since February 10, 2012.

<span class="mw-page-title-main">ROMK</span> Potassium channel

The renal outer medullary potassium channel (ROMK) is an ATP-dependent potassium channel (Kir1.1) that transports potassium out of cells. It plays an important role in potassium recycling in the thick ascending limb (TAL) and potassium secretion in the cortical collecting duct (CCD) of the nephron. In humans, ROMK is encoded by the KCNJ1 gene. Multiple transcript variants encoding different isoforms have been found for this gene.

Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body. It can result in multiple symptoms. Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus. Complications may include seizures or cardiac arrest such as from torsade de pointes. Those with low magnesium often have low potassium.

<span class="mw-page-title-main">Pseudohypoaldosteronism</span> Medical condition

Pseudohypoaldosteronism (PHA) is a condition that mimics hypoaldosteronism. However, the condition is due to a failure of response to aldosterone, and levels of aldosterone are actually elevated, due to a lack of feedback inhibition.

<span class="mw-page-title-main">KCNE2</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel subfamily E member 2 (KCNE2), also known as MinK-related peptide 1 (MiRP1), is a protein that in humans is encoded by the KCNE2 gene on chromosome 21. MiRP1 is a voltage-gated potassium channel accessory subunit associated with Long QT syndrome. It is ubiquitously expressed in many tissues and cell types. Because of this and its ability to regulate multiple different ion channels, KCNE2 exerts considerable influence on a number of cell types and tissues. Human KCNE2 is a member of the five-strong family of human KCNE genes. KCNE proteins contain a single membrane-spanning region, extracellular N-terminal and intracellular C-terminal. KCNE proteins have been widely studied for their roles in the heart and in genetic predisposition to inherited cardiac arrhythmias. The KCNE2 gene also contains one of 27 SNPs associated with increased risk of coronary artery disease. More recently, roles for KCNE proteins in a variety of non-cardiac tissues have also been explored.

<span class="mw-page-title-main">Cation channel superfamily</span> Family of ion channel proteins

The transmembrane cation channel superfamily was defined in InterPro and Pfam as the family of tetrameric ion channels. These include the sodium, potassium, calcium, ryanodine receptor, HCN, CNG, CatSper, and TRP channels. This large group of ion channels apparently includes families 1.A.1, 1.A.2, 1.A.3, and 1.A.4 of the TCDB transporter classification.

<span class="mw-page-title-main">KCND2</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel subfamily D member 2 is a protein that in humans is encoded by the KCND2 gene. It contributes to the cardiac transient outward potassium current (Ito1), the main contributing current to the repolarizing phase 1 of the cardiac action potential.

<span class="mw-page-title-main">KCNA2</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel subfamily A member 2 also known as Kv1.2 is a protein that in humans is encoded by the KCNA2 gene.

<span class="mw-page-title-main">KCNA3</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel, shaker-related subfamily, member 3, also known as KCNA3 or Kv1.3, is a protein that in humans is encoded by the KCNA3 gene.

<span class="mw-page-title-main">KCNE4</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel subfamily E member 4, originally named MinK-related peptide 3 or MiRP3 when it was discovered, is a protein that in humans is encoded by the KCNE4 gene.

<span class="mw-page-title-main">Anion exchange transporter</span> Protein-coding gene in the species Homo sapiens

Anion exchange transporter is a protein that in humans is encoded by the SLC26A7 gene.

<span class="mw-page-title-main">KCNA10</span> Protein-coding gene in the species Homo sapiens

Potassium voltage-gated channel subfamily A member 10 also known as Kv1.8 is a protein that in humans is encoded by the KCNA10 gene. The protein encoded by this gene is a voltage-gated potassium channel subunit.

<span class="mw-page-title-main">KCNAB3</span> Protein-coding gene in the species Homo sapiens

Voltage-gated potassium channel subunit beta-3 is a protein that in humans is encoded by the KCNAB3 gene. The protein encoded by this gene is a voltage-gated potassium channel beta subunit.

<span class="mw-page-title-main">Stichodactyla toxin</span> Protein family

Stichodactyla toxin is a 35-residue basic peptide from the sea anemone Stichodactyla helianthus that blocks a number of potassium channels. Related peptides form a conserved family of protein domains known as the ShkT domain. Another well-studied toxin of the family is BgK from Bunodosoma granulifera.

<span class="mw-page-title-main">Renalase</span> Mammalian protein found in Homo sapiens

Renalase, FAD-dependent amine oxidase is an enzyme that in humans is encoded by the RNLS gene. Renalase is a flavin adenine dinucleotide-dependent amine oxidase that is secreted into the blood from the kidney.

<span class="mw-page-title-main">Roxadustat</span> Anti-anemia medication

Roxadustat, sold under the brand name Evrenzo, is an anti-anemia medication. Roxadustat is a HIF prolyl-hydroxylase inhibitor that increases endogenous production of erythropoietin and stimulates production of hemoglobin and red blood cells. It was investigated in clinical trials for the treatment of anemia caused by chronic kidney disease (CKD). It is taken by mouth. The drug was developed by FibroGen, in partnership with AstraZeneca.

References

  1. ↑ "Deborah E. Dyett And Gary DeSir Set Bridal for Aug. 26". The New York Times. 1979-04-08. ISSN   0362-4331 . Retrieved 2021-09-29.
  2. ↑ "Theta Epsilon Omega Chapter - Deborah Dyett Desir, MD, Joins ACR Executive Committee as Secretary". www.akanewhaven.org. Retrieved 2021-09-29.
  3. ↑ Parry, Julie. "Desir Named Vice Provost for Faculty Development and Diversity". medicine.yale.edu. Retrieved 2021-09-17.
  4. ↑ "Founders Day: Building a Stronger and More Inclusive Yale". Office of the President. 2020-10-14. Retrieved 2021-09-17.
  5. ↑ Stevens, Chester (2020-10-14). "Salovey unveils new plans for equity, belonging at Yale". University News HQ. Retrieved 2021-09-17.
  6. ↑ "amhe.org" . Retrieved 2021-09-17.
  7. ↑ "Kidney enzyme renalase a potential therapy for severe COVID-19". News-Medical.net. 2020-06-07. Retrieved 2021-09-17.
  8. ↑ "What is Renalase?". News-Medical.net. 2020-07-01. Retrieved 2021-09-17.
  9. ↑ Guo, Xiaojia; Hollander, Lindsay; MacPherson, Douglas; Wang, Ling; Velazquez, Heino; Chang, John; Safirstein, Robert; Cha, Charles; Gorelick, Fred; Desir, Gary V. (2016-03-14). "Inhibition of renalase expression and signaling has antitumor activity in pancreatic cancer". Scientific Reports. 6 (1): 22996. Bibcode:2016NatSR...622996G. doi:10.1038/srep22996. ISSN   2045-2322. PMC   4789641 . PMID   26972355.
  10. ↑ Parry, Julie. "Desir Shares Life Story, Advice in "The Importance of Being Present"". medicine.yale.edu. Retrieved 2021-09-17.
  11. ↑ "Gary V. Desir, M.D., appointed Chair and Chief of Internal Medicine". medicine.yale.edu. Retrieved 2021-09-17.
  12. ↑ "Gary Desir, MD". medicine.yale.edu. Retrieved 2021-09-17.
  13. ↑ "Gary V. Desir, M.D., appointed Chair and Chief of Internal Medicine". medicine.yale.edu. Retrieved 2021-09-17.
  14. ↑ "Gary V. Desir, M.D., HS '83, FW '87, named interim chair of internal medicine". medicine.yale.edu. Retrieved 2021-09-17.
  15. ↑ "More news about Yale people". yalealumnimagazine.com. Retrieved 2021-09-17.
  16. ↑ "Dr. Gary Desir designated the Beeson Professor of Internal Medicine". YaleNews. 2016-09-06. Retrieved 2021-09-17.
  17. ↑ "DIM Comp R2". Issuu. Retrieved 2021-09-29.
  18. ↑ Sanger, Catherine Shea; Gleason, Nancy W., eds. (2020). Diversity and Inclusion in Global Higher Education. doi:10.1007/978-981-15-1628-3. ISBN   978-981-15-1627-6. S2CID   237868497.
  19. ↑ "Gary Desir". Yale Medicine. Retrieved 2021-09-17.
  20. ↑ Desir, Gary (2012). "Novel insights into the physiology of renalase and its role in hypertension and heart disease". Pediatric Nephrology (Berlin, Germany). 27 (5): 719–725. doi:10.1007/s00467-011-1828-7. ISSN   1432-198X. PMID   21424526. S2CID   8473507.
  21. ↑ Desir, Gary. "Renalase Deficiency and Cardiovascular Complications of Chronic Kidney Disease".{{cite journal}}: Cite journal requires |journal= (help)
  22. ↑ Castillo, Grace (2016-03-29). "Potential treatment for pancreatic cancer on horizon". Yale Daily News. Retrieved 2021-09-17.
  23. ↑ "AMHE Newsletter. In this number. Winter Haitian Medical Association Abroad Association Medicale Haïtienne à l'étranger. - PDF Free Download". docplayer.fr. Retrieved 2021-09-17.
  24. ↑ Guo, Xiaojia; Hollander, Lindsay; MacPherson, Douglas; Wang, Ling; Velazquez, Heino; Chang, John; Safirstein, Robert; Cha, Charles; Gorelick, Fred; Desir, Gary V. (2016-03-14). "Inhibition of renalase expression and signaling has antitumor activity in pancreatic cancer". Scientific Reports. 6 (1): 22996. Bibcode:2016NatSR...622996G. doi:10.1038/srep22996. ISSN   2045-2322. PMC   4789641 . PMID   26972355.
  25. ↑ Wang, Yang; Safirstein, Robert; Velazquez, Heino; Guo, Xiao‐Jia; Hollander, Lindsay; Chang, John; Chen, Tian‐Min; Mu, Jian‐Jun; Desir, Gary V. (2017). "Extracellular renalase protects cells and organs by outside‐in signalling". Journal of Cellular and Molecular Medicine. 21 (7): 1260–1265. doi:10.1111/jcmm.13062. ISSN   1582-1838. PMC   5487909 . PMID   28238213.
  26. ↑ "Blood protein predicts poor COVID-19 outcomes". medicalxpress.com. Retrieved 2021-09-17.
  27. ↑ "Kidney enzyme renalase a potential therapy for severe COVID-19". News-Medical.net. 2020-06-07. Retrieved 2021-09-17.
  28. ↑ Parry, Julie. "Diversity, Equity, Inclusion Focus Of Department of Internal Medicine". medicine.yale.edu. Retrieved 2021-09-17.
  29. ↑ "Who We Are". medicine.yale.edu. Retrieved 2021-09-17.
  30. ↑ ""Black Women in Medicine" Documentary to Screen at Yale on Tuesday 4/26". Good Black News. 2016-04-24. Retrieved 2021-09-17.
  31. ↑ Xiong, Amy (2018-03-30). "Global Health Day addresses climate change". Yale Daily News. Retrieved 2021-09-17.
  32. ↑ Xu, Jianchao; Li, Guoyong; Wang, Peili; Velazquez, Heino; Yao, Xiaoqiang; Li, Yanyan; Wu, Yanling; Peixoto, Aldo; Crowley, Susan; Desir, Gary V. (2005-05-02). "Renalase is a novel, soluble monoamine oxidase that regulates cardiac function and blood pressure". Journal of Clinical Investigation. 115 (5): 1275–1280. doi:10.1172/JCI24066. ISSN   0021-9738. PMC   1074681 . PMID   15841207.
  33. ↑ Gutman, George A.; Chandy, K. George; Adelman, John P.; Aiyar, Jayashree; Bayliss, Douglas A.; Clapham, David E.; Covarriubias, Manuel; Desir, Gary V.; Furuichi, Kiyoshi; Ganetzky, Barry; Garcia, Maria L. (2003-12-01). "International Union of Pharmacology. XLI. Compendium of Voltage-Gated Ion Channels: Potassium Channels". Pharmacological Reviews. 55 (4): 583–586. doi:10.1124/pr.55.4.9. PMID   14657415. S2CID   34963430.
  34. ↑ Hebert, Steven C.; Desir, Gary; Giebisch, Gerhard; Wang, Wenhui (2005-01-01). "Molecular Diversity and Regulation of Renal Potassium Channels". Physiological Reviews. 85 (1): 319–371. doi:10.1152/physrev.00051.2003. ISSN   0031-9333. PMC   2838721 . PMID   15618483.
  35. ↑ Li, Guoyong; Xu, Jianchao; Wang, Peili; Velazquez, Heino; Li, Yanyan; Wu, Yanling; Desir, Gary V. (2008-03-11). "Catecholamines Regulate the Activity, Secretion, and Synthesis of Renalase". Circulation. 117 (10): 1277–1282. doi: 10.1161/CIRCULATIONAHA.107.732032 . PMID   18299506. S2CID   6658935.
  36. ↑ Xu, Jianchao; Wang, Peili; Li, Yanyan; Li, Guoyong; Kaczmarek, Leonard K.; Wu, Yanling; Koni, Pandelakis A.; Flavell, Richard A.; Desir, Gary V. (2004-03-02). "The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity". Proceedings of the National Academy of Sciences. 101 (9): 3112–3117. Bibcode:2004PNAS..101.3112X. doi: 10.1073/pnas.0308450100 . PMC   365752 . PMID   14981264.
  37. ↑ Xu, J. (2003-03-01). "The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight". Human Molecular Genetics. 12 (5): 551–559. doi: 10.1093/hmg/ddg049 . ISSN   1460-2083. PMID   12588802.
  38. ↑ Kunchaparty, Shanti; Palcso, Matthew; Berkman, Jennifer; Velázquez, Heino; Desir, Gary V.; Bernstein, Paul; Reilly, Robert F.; Ellison, David H. (1999-10-01). "Defective processing and expression of thiazide-sensitive Na-Cl cotransporter as a cause of Gitelman's syndrome". American Journal of Physiology. Renal Physiology. 277 (4): F643–F649. doi:10.1152/ajprenal.1999.277.4.F643. ISSN   1931-857X. PMID   10516289.
  39. ↑ Desir, Gary V. (2009). "Regulation of blood pressure and cardiovascular function by renalase". Kidney International. 76 (4): 366–370. doi: 10.1038/ki.2009.169 . ISSN   0085-2538. PMID   19471322.
  40. ↑ Desir, Gary V.; Tang, LieQi; Wang, Peili; Li, Guoyong; Sampaio‐Maia, Benedita; Quelhas‐Santos, Janete; Pestana, Manuel; Velazquez, Heino (2012). "Renalase Lowers Ambulatory Blood Pressure by Metabolizing Circulating Adrenaline". Journal of the American Heart Association. 1 (4): e002634. doi:10.1161/JAHA.112.002634. PMC   3487338 . PMID   23130169.
  41. ↑ Farzaneh-Far, Ramin; Desir, Gary V.; Na, Beeya; Schiller, Nelson B.; Whooley, Mary A. (2010-10-20). "A Functional Polymorphism in Renalase (Glu37Asp) Is Associated with Cardiac Hypertrophy, Dysfunction, and Ischemia: Data from the Heart and Soul Study". PLOS ONE. 5 (10): e13496. Bibcode:2010PLoSO...513496F. doi: 10.1371/journal.pone.0013496 . ISSN   1932-6203. PMC   2958117 . PMID   20975995.
  42. ↑ Desir, Gary V.; Peixoto, Aldo J. (2013-10-17). "Renalase in hypertension and kidney disease". Nephrology Dialysis Transplantation. 29 (1): 22–28. doi: 10.1093/ndt/gft083 . ISSN   1460-2385. PMID   24137013.
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