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Nithya Mariappan

Researcher at Louisiana State University

Publications -  23
Citations -  1683

Nithya Mariappan is an academic researcher from Louisiana State University. The author has contributed to research in topics: Oxidative stress & Reactive oxygen species. The author has an hindex of 16, co-authored 20 publications receiving 1521 citations. Previous affiliations of Nithya Mariappan include University of Alabama at Birmingham.

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NF-κB-induced oxidative stress contributes to mitochondrial and cardiac dysfunction in type II diabetes

TL;DR: This study demonstrates that NF-kappaB blockade with PDTC mitigates oxidative stress and improves mitochondrial structural integrity directly, through down-regulation of increased oxygen-free radicals, thereby increasing ATP synthesis and thus restoring cardiac function in type II diabetes.
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HDAC inhibition attenuates inflammatory, hypertrophic, and hypertensive responses in spontaneously hypertensive rats

TL;DR: Data indicate that long-term histone deacetylase inhibition, independent of the blood pressure response, reduces hypertrophic, proinflammatory, and hypertensive responses by decreasing reactive oxygen species and angiotensin II type1 receptor expression in the heart, demonstrating the importance of uncontrolled Histone de acetylase activity in hypertension.
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TNF-α-induced mitochondrial oxidative stress and cardiac dysfunction : restoration by superoxide dismutase mimetic Tempol

TL;DR: The studies demonstrate that TNF-alpha-induced oxidative stress alters redox homeostasis by impairing the MPTP proteins adenine nucleotide translocator and voltage-dependent anion channel, thereby resulting in the pore opening, causing uncontrolled transport of substances to alter mitochondrial pH, and subsequently leading to dysfunction of mitochondria and attenuated cardiac function.
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Angiotensin II–Induced Hypertension Is Modulated by Nuclear Factor-κB in the Paraventricular Nucleus

TL;DR: The important role that transcription factor NF&kgr;B plays within the PVN in modulating and perpetuating the hypertensive response via renin-angiotensin system modulation is demonstrated.