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T R Santhosh Kumar, PhD

Scientist E-II

+91-471-2529500

trsanthosh@rgcb.res.in

santhoshkumar
santhoshkumar

T R Santhosh Kumar, PhD

Scientist E-II

+91-471-2529500

trsanthosh@rgcb.res.in

  • Profile

    • Ph.D (Sree Chitra Thirunal Institute for Medical Sciences & Technology)
  • Research

    Molecular mechanisms involved in mitochondrial bioenergetics dys-regulation in heart failure associated with aging.

    Fifty percent of all heart failure diseases and 90% of all heart failure deaths occur in individuals above 70 years of age. Aging is generally characterized by a decline in physiological functioning and increased susceptibility to diseases. The mechanism by which the basic biology of aging drives chronic diseases prevalent among the older population is still vague. From the molecular and cellular analysis studies, it has been suggested that there are multiple interaction between aging and disease variables. As telomere dys-functioning may lead to the activation of p53- PGC1α/β pathway which further impairs overall mitochondrial biogenesis and function, defective ATP generation and increased level of reactive oxygen species (ROS) might contribute to aging pathologies. During premature aging/progeroid syndromes such as progeria, Werner syndrome, and ataxia telangiectasia, defective p53-DNA damage pathway, and accumulation of defective protein/ proteostasis like progerin as seen in progeria are found to be involved. My interest is to understand the physiological and molecular mechanisms involved in the dysregulation of metabolism and interacellular bioenergetics which might lead to heart failure associated with aging. This study is expected to answer whether or not it is possible to prevent or retard the aging effects on the heart that contribute to development of cardiac failure. I wish to find whether age related haemodynamic changes might lead to decline in mitochondrial metabolic function and telomere dysfunction and contribute to heart failure.

  • Publications

  • Team


    Vikas Panchal, Senior Research Fellow

    Molecular mechanisms involved in mitochondrial bioenergetics dys-regulation in heart failure associated with aging.

    Fifty percent of all heart failure diseases and 90% of all heart failure deaths occur in individuals above 70 years of age. Aging is generally characterized by a decline in physiological functioning and increased susceptibility to diseases. The mechanism by which the basic biology of aging drives chronic diseases prevalent among the older population is still vague. From the molecular and cellular analysis studies, it has been suggested that there are multiple interaction between aging and disease variables. As telomere dys-functioning may lead to the activation of p53- PGC1α/β pathway which further impairs overall mitochondrial biogenesis and function, defective ATP generation and increased level of reactive oxygen species (ROS) might contribute to aging pathologies. During premature aging/progeroid syndromes such as progeria, Werner syndrome, and ataxia telangiectasia, defective p53-DNA damage pathway, and accumulation of defective protein/ proteostasis like progerin as seen in progeria are found to be involved. My interest is to understand the physiological and molecular mechanisms involved in the dysregulation of metabolism and interacellular bioenergetics which might lead to heart failure associated with aging. This study is expected to answer whether or not it is possible to prevent or retard the aging effects on the heart that contribute to development of cardiac failure. I wish to find whether age related haemodynamic changes might lead to decline in mitochondrial metabolic function and telomere dysfunction and contribute to heart failure.

    vikas
    vikas

    Vikas Panchal, Senior Research Fellow

    Molecular mechanisms involved in mitochondrial bioenergetics dys-regulation in heart failure associated with aging.

    Fifty percent of all heart failure diseases and 90% of all heart failure deaths occur in individuals above 70 years of age. Aging is generally characterized by a decline in physiological functioning and increased susceptibility to diseases. The mechanism by which the basic biology of aging drives chronic diseases prevalent among the older population is still vague. From the molecular and cellular analysis studies, it has been suggested that there are multiple interaction between aging and disease variables. As telomere dys-functioning may lead to the activation of p53- PGC1α/β pathway which further impairs overall mitochondrial biogenesis and function, defective ATP generation and increased level of reactive oxygen species (ROS) might contribute to aging pathologies. During premature aging/progeroid syndromes such as progeria, Werner syndrome, and ataxia telangiectasia, defective p53-DNA damage pathway, and accumulation of defective protein/ proteostasis like progerin as seen in progeria are found to be involved. My interest is to understand the physiological and molecular mechanisms involved in the dysregulation of metabolism and interacellular bioenergetics which might lead to heart failure associated with aging. This study is expected to answer whether or not it is possible to prevent or retard the aging effects on the heart that contribute to development of cardiac failure. I wish to find whether age related haemodynamic changes might lead to decline in mitochondrial metabolic function and telomere dysfunction and contribute to heart failure.

  • Alumni