Shakila Mahalakshmi

Senior Research Fellow

Diabetes is the killer metabolic disorder leading to most of the complications such as cardiopathy, nephropathy, and neuropathy. Chronic diabetes leads to cardiomyopathy in which the heart undergoes ventricular remodelling due to hypertrophy and fibrosis. Such patients affected with coronary blockages have to undergo procedures such as CABG and PCI which lead to revascularisation injury. Recent research has suggested that the classical protective pathways are modified or ineffective in hearts affected by diabetic cardiomyopathy. My present work compares these signalling pathways in the early stages of diabetes and its progression in the late stages.

Sriram

Junior Research Fellow

Recent studies on post CABG patients (Nah et.al., 2014) have revealed that 27% of them have new brain infarcts located silently and cortically, leading to cryptogenic stroke. Ishikawa and co-workers in 2013 have proved that supernatant from ischemia reperfusion induced neuronal cells lead to massive death in cardiac cell, indicating a close pathological link between brain and heart. The exact mechanism behind this phenomenon could not be explained except that an elevation of cell death markers was reported followed by a reduction in mitochondrial reductase (MTT) activity. The existence of distinct subpopulations of mitochondria in heart namely interfibrillar (IFM) and subsarcolemmal mitochondria (SSM), with differences among their complex enzyme activities and tolerance towards ischemic insult needs further exploration. Additionally the regional differences among the brain mitochondria with respect to cortex, hippocampus and striatum, showing variations in vulnerability towards the ischemic insult starting from the ischemic core towards the penumbra have posed a challenge in treatment of stroke. Despite of several trials from 1971 in this field, no drug has successfully been translated to clinical effectiveness to date. This leaves us with the only option of treating with mechanically conditioning the ischemia. My focus of the present study is to explore the end/remote/distant organ that is affected due to revascularization injury. More specifically this study is designed to identify the mitochondrial dysfunction in the heart, affected due to revascularization of brain and vice versa. The ultimate goal is to therapeutically target mitochondria in all these organs and improve its function thereby preserving the organ, long term cognition and survival of patients undergoing cardiac bypass. With respect to current knowledge in the field, this study aims to determine the vulnerability of mitochondrial subpopulations towards the injury, to design target specific drugs and replace the dead mitochondria by new ones or promoting biogenesis using cell based approaches

Sri Rahavi

Junior Research Fellow

My interest is focused on how the gasotransmitters affect the recovery of heart from MIRI. As these molecules are gaseous in nature, they tend to have an interconnection with the signalling pathways involved in pathology of MIRI. It is known that mitochondrial dysfunction plays a major role in pathology of this condition and the existence of two sub-populations in heart having a differential impact makes the study in this field more interesting. I am interested in studying the interplay between the gasotransmitters and their impact on the two cardiac mitochondrial sub-populations – IFM and SSM. I work with both cell line models and animal models.

Priyanka

CSIR-Junior Research Fellow

Ischemia of one or both kidneys is also a common problem experienced during aortic surgery involving clamping of the aorta and/or renal arteries, e.g., surgery for supra- and juxtarenal abdominal aortic aneurysms, renal transplantation, or during cardiovascular anaesthesia, leading to significant postoperative complications including the development of ischemic AKI (Acute Kidney Injury). In organ transplantation, as well as in major surgery IRI(Ischemia Reperfusion Injury) is a relevant challenge, which importantly influences the clinical outcome. In high-risk patients undergoing these forms of surgery, the incidence of renal dysfunction has been reported to be as high as 50%. So preventing IRI will improve the graft survival after organ transplantation. The intracellular and molecular mechanisms involved in the development of renal IR injury are complex and not yet fully understood. Our experiments focus on understanding the mechanism behind Renal IRI and try to find methods to minimize IRI either before, during or after ischemia.

Bhavana

Junior Research Fellow

Today, air pollution has become a global public health problem and is recognized as a major environmental health hazard by agencies such as the WHO and governments around the world. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter(PM 2.5 and PM 10) and gases(carbon monoxide, nitrogen oxides ,sulfur dioxide and carbon dioxide). I am interested in understanding the influence of Air pollutants (PM, organic and inorganic gases, indoor pollutants) on Ischemic heart disease. More specifically I will be checking if exposure to air pollutants aggregates the cardiomyocyte injury or not through In vitro, In vivo and population based studies.

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