Dr. Bhuiyan's lab has received an NIH R01 grant from the National Institutes of Health titled “Sigmar1 in lipid metabolism.” Dr. Bhuiyan’s proposal will investigate a novel function of a protein named Sigma-1 receptor (Sigmar1) in regulating lipid metabolism in baseline and in response to diet-induced obesity. The goal of this application is to discover a novel lipid metabolism pathway regulated by Sigmar1 and identify a therapeutic target to prevent lipid abnormalities in obesity, which is expected to help reverse the impact of obesity on cardiovascular disease risk.

Shafiul Alam, PhD, Postdoctoral Fellow, was awarded an American Heart Association Postdoctoral Fellowship award of $106,532 for his two-year project (7/2018-6/2020),  “Sigmar1 autophagic function in protecting cardiac proteotoxicity.”

Chowdhury S Abdullah, PhD, Postdoctoral fellow got 2018 BCVS Abstract Travel Grant from the AHA’s Scientific Session held in Chicago, Illinois (November 10–12, 2018).  

Chowdhury S Abdullah, PhD, Postdoctoral fellow got the BCVS Young Investigator Travel Award at the Basic Cardiovascular Sciences (BCVS) Scientific Session held in San Antonio, TX (Jul 30 - Aug 02, 2018).  

Shafiul Alam, PhD, Postdoctoral fellow got the BCVS Young Investigator Travel Award at the Basic Cardiovascular Sciences (BCVS) Scientific Session held in San Antonio, TX (Jul 30 - Aug 02, 2018)  

Chowdhury S. Abdullah, PhD, Postdoctoral fellow got the Early Career Investigator (ECI) Travel Award on the 36th Annual Meeting of the North American Section of International Society for Heart Research (ISHR), New Orleans, LA (May 30 - Jun 2, 2017).

Shafiul Alam, PhD, Postdoctoral fellow got the Early Career Investigator (ECI) Travel Award on the 36th Annual Meeting of the North American Section of International Society for Heart Research (ISHR), New Orleans, LA (May 30 - Jun 2, 2017).
 

Sigmar1’s Function in the Heart:
My overarching research goal is to elucidate novel physiological functions of Sigma-1 receptor (Sigmar1) in the heart and to discover its cardioprotective functions during adverse cardiac remodeling and failure, using integrated molecular, genetic and functional approaches in genetically modified mice. Over the years, I have developed all the genetic tools including Sigmar1 cardiac-specific transgenic mouse, conditional transgenic mouse and also knockout mouse to investigate for the first time the pathophysiological role of Sigmar1 in cardiac biology. Through the use of these new genetic tools, we will be able to discover novel signaling mechanisms and therapeutic approach for singularly manipulating heart failure in mice in vivo.  My lab uses integrated approaches in molecular cardiovascular biology need to study ischemia/reperfusion-injury, transverse aortic constriction-induced and genetic models of heart failure including cardiac functional analysis such as echocardiography, invasive hemodynamics, and blood pressure measurements. 

Functional Significance of Autophagy in Cardiac Physiology: 
Basal autophagy is a crucial mechanism of cellular homeostasis, underlying both normal cellular recycling and the clearance of damaged or misfolded proteins, organelles, and aggregates. Due to the potential importance of autophagy in biological processes, my research is particularly focused on understanding its roles during cardiac disease. My lab uses a combination of genetic autophagy reporter mice and cardiac-specific inducible autophagy mouse to define the effects of acute or chronic increased basal autophagy in the heart. Our recent research projects aimed at investigating the pathophysiological role of mitochondrial autophagy and mitochondrial bioenergetics in cardiac biology using new genetic tools for singularly manipulating heart failure in mice.

Discovering novel therapies to treat obesity and metabolic diseases:
Obesity is a serious concern because it increases the risk of cardiovascular disease among other health problems and particularly responsible for death in patients with heart failure. Uncorrected prolonged severe obesity predisposes individuals to myocardial damage characterized as cardiac hypertrophy and contractile dysfunction eventually leading to the development of heart failure. Extensive studies on obesity associated-cardiac dysfunction demonstrate several theories including alterations in myocardial substrate utilization, neurohumoral activation, mitochondrial dysfunction, oxidative stress, impaired insulin signaling, and lipotoxicity, but the underlying pathological mechanisms remain elusive. My lab is vested in identifying novel therapies and discovering the molecular signaling pathways responsible for obesity-induced cardiac dysfunction for therapeutic intervention. 

Cancer treatment-related cardiotoxicity:
Anthracyclines (e.g., Doxorubicin) and related anticancer drugs are widely used for treating human cancers, but can induce heart failure through an undefined mechanism. Extensive studies over the half-century revealed that Doxorubicin-induced cardiotoxic effects were associated with accumulation of dysfunctional mitochondria, generation of reactive oxygen species (ROS), initiation of mitochondrial oxidative stress, mitochondrial injury, and cell death. My lab is using genetic mouse models to discover the molecular signaling pathways responsible for anticancer drug treatment-induced cardiac dysfunction for therapeutic intervention. 

Ovarian Hormones and Cardiac Stress Response:
Incidence of cardiovascular disease is higher in men than in premenopausal women but increases in postmenopausal women. Cardiovascular diseases are the leading causes of morbidity and mortality among postmenopausal women and account for nearly half of all deaths in women. My research aims to generate as well as to characterize a model of postmenopausal cardiac decompensation and to elucidate the molecular mechanisms that contribute to the effects of menopause on left ventricular hypertrophy.

Selected Publications (26 total)

1. Aishwarya R, Abdullah CS, Remex NS, Nitu S, Hartman B, King J, Bhuiyan MAN, Rom O, Miriyala S, Panchatcharam M, Orr AW, Kevil CG, Bhuiyan MS. Pathological sequelae associated with skeletal muscle atrophy and histopathology in G93A*SOD1 mouse. Muscles. 2023; 2(1): 51-74; https://doi.org/10.3390/muscles2010006.

2. Tagashira H, Bhuiyan MS, Shinoda Y, Kawahata I, Numata T, Fukunaga K. Sigma-1 receptor is involved in modification of ER-mitochondrial proximity and Ca2+ homeostasis in cardiomyocytes. J Pharmacol Sci. 2023 Feb;151(2):128-133. doi: 10.1016/j.jphs.2022.12.005.

   Abdullah CS, Alam S, Aishwarya T, Miriyala S, Bhuiyan MAN, Panchatcharam M, Pattillo CB, Orr AW, Sadoshima J, Hill JA, Bhuiyan MS. Doxorubicin-induced cardiomyopathy associated with inhibition of autophagic degradation process and defects in mitochondrial respiration. Sci Rep. 2019 Feb 14;9(1):2002. doi: 10.1038/s41598-018-37862-3.
3. Abdullah CS, Alam S, Aishwarya T, Miriyala S, Panchatcharam M, Bhuiyan MAN, Peretik JM, Orr AW, James J, Osinska H, Robbins J, Lorenz JN, Bhuiyan MS. Cardiac dysfunction in the Sigmar1 knockout mouse associated with impaired mitochondrial dynamics and bioenergetics. J Am Heart Assoc. 2018;7:e009775 DOI: 10.1161/JAHA.118.009775.
4. Alam S, Abdullah CS, Aishwarya T, Miriyala S, Panchatcharam M, Peretik JM, Orr AW, James J, Robbins J, Bhuiyan MS. Aberrant mitochondrial fission is maladaptive in Desmin mutation-induced cardiac proteotoxicity. J Am Heart Assoc. 2018;7:e009289. DOI: 10.1161/JAHA.118.009289.
5. Alam S, Abdullah CS, Aishwarya R, Orr AW, Traylor J, Miriyala S, Panchatcharam M, Pattillo CB, Bhuiyan MS. Sigmar1 regulates endoplasmic reticulum stress-induced C/EBP-homologous protein expression in cardiomyocytes. Biosci Rep. 2017 Jul 16;37(4). pii: BSR20170898. doi: 10.1042/BSR20170898. Print 2017 Aug 31. PMID:28667101. 
6. Bhuiyan MS, McLendon P, James J, Osinska H, Gulick J, Bhandary B, Lorenz JN, Robbins J. In vivo definition of cardiac myosin-binding protein C's critical interactions with myosin. Pflugers Arch 2016;468 (10):685–1695.
7. Bhuiyan MS, Pattison JS, Osinska H, James J, Gulick J, McLendon PM, Hill JA, Sadoshima J, Robbins J. Enhanced autophagy ameliorates cardiac proteinopathy. J Clin Invest 2013;123(12):5284-97.
8. Bhuiyan MS, Gulick J, Osinska H, Gupta M, Robbins J. Determination of the critical residues responsible for cardiac myosin binding protein C's interactions. J Mol Cell Cardiol. 2012;53(6):838-847.
9. Bhuiyan MS, Tagashira H, Fukunaga K.Sigma-1 receptor stimulation with fluvoxamine ameliorates pressure overload-induced hypertrophy and dysfunctions in ovariectomized rats.  Expert Opin Ther Targets 2010;14(10):1009-22.
10. Bhuiyan MS, Fukunaga K. Stimulation of Sigma-1 receptor signaling by dehydroepiandrosterone ameliorates pressure overload-induced hypertrophy and dysfunctions in ovariectomized rats. Expert Opin Ther Targets 2009;13(11):1253-1265.
11. Bhuiyan MS, Shioda N, Fukunaga K. Chronic β-AR activation-induced calpain activation and impaired eNOS-Akt signaling mediates cardiac injury in ovariectomized in female rats. Expert Opin Ther Targets 2009;13(3):275-286.
12. Bhuiyan MS, Shioda N, Shibuya M, Iwabuchi Y, Fukunaga K. Activation of endothelial nitric oxide synthase by a vanadium compound ameliorates pressure overload-induced cardiac injury in ovariectomized rats. Hypertension 2009;53(1):57-63.
13. Bhuiyan MS, Takada Y, Shioda N, Moriguchi S, Kasahara J and Fukunaga K. Cardioprotective effect of vanadyl sulfate on ischemia/reperfusion-induced injury in rat heart in vivo is mediated by activation of protein kinase B and induction of FLICE-inhibitory protein. Cardiovasc Ther 2008;26(1):10-23.
14. Bhuiyan MS, Shioda N, Fukunaga K. Ovariectomy augments pressure overload-induced hypertrophy associated with changes in Akt and nitric oxide synthase signaling pathways in female rats. Am J Physiol Endocrinol Metab 2007;293(6): E1606-1614.
15. Bhuiyan MS, Fukunaga K. Inhibition of HtrA2/Omi ameliorates heart dysfunction following ischemia/reperfusion injury in rat hearts in vivo. Eur J Pharmacol 2007;557(2-3):168-177.

Complete List of Published Work in My Bibliography
(total 26 publications, 20 first author): http://1.usa.gov/1NXz3qy

Post-doctoral Fellows

We are not actively recruiting Postdoctoral Fellows but exceptional applicants will always be considered. Interested applicants should submit a CV listing three references to Dr. Bhuiyan at mbhuiy@lsuhsc.edu.

Graduate Students

Graduate students interested in conducting research in the Bhuiyan lab should review the current laboratory research directions and contact Dr. Bhuiyan at mbhuiy@lsuhsc.edu.

Undergraduate Research Assistants

We are not currently hiring any additional undergraduates. However, positions can become available during the summer.
 

Contact the Bhuiyan Lab

LSU Health Shreveport
Department of Pathology
1501 Kings Hwy
Shreveport, LA 71103

Phone:
(318) 675-3369 office
(318) 675-3368 lab
(318) 675-8144 fax
E-mail: shenu.bhuiyan@lsuhs.edu