Publications by authors named "S K Mohanta"

Recent research has advanced the understanding of atherosclerosis as a transmural chronic inflammatory disease involving all three layers of the arterial wall, including the intima plaque, the media, and the adventitia, which forms the outer connective tissue coat of arteries. Our recent studies have suggested that the adventitia is used by the peripheral nervous system as a conduit for reaching all tissue cells. We also found that the peripheral nervous system, that is, the sensory and sympathetic nervous system, undergoes major remodeling processes involving the neogenesis of axon networks adjacent to atherosclerotic plaques.

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TRPV1, a polymodal and nonselective cation channel has unique gating mechanisms which is regulated by supramolecular complexes at the plasma membrane formed with membrane proteins, lipids and kinase pathways. Crosstalk between microtubule cytoskeleton with TRPV1 at various level has been established. Previously we demonstrated that the positively-charged residues present at specific tubulin-binding stretch sequences (i.

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Article Synopsis
  • * Early intermittent feeding of mice on a high-cholesterol diet speeds up atherosclerosis by altering arterial macrophage behavior and gene expression associated with ASCVD.
  • * The Young Finns Study links early cholesterol exposure to increased carotid atherosclerotic plaque in adulthood, emphasizing the need for better hyperlipidaemia management early in life to prevent ASCVD.
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Microtubule-based chemotherapeutics, primarily Taxane-derived agents are still used as the major live-saving agents, yet have several side effects including serious loss of immune cells, bone density etc. which lowers the quality of life. This imposes the need to understand the effects of these agents on Mesenchymal Stem Cells (MSCs) in details.

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Article Synopsis
  • TRPV1 is a unique ion channel with distinct structural properties, and the mutant TRPV1-R575D shows reduced interaction with membrane cholesterol, leading to "ligand-insensitivity" and high cellular lethality under control conditions.
  • The lethality from TRPV1-R575D can be mitigated by using a specific inhibitor (5'I-RTX) or by introducing a second mutation (D576R) near R575D.
  • The study reveals that conditions like lowering extracellular Ca or depleting membrane cholesterol can rescue the "ligand-insensitivity" of TRPV1-R575D and highlights the importance of intracellular calcium for channel gating in both the wild type and mutant forms.
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