R
Riya R. Kanherkar
Researcher at Howard University
Publications - 7
Citations - 587
Riya R. Kanherkar is an academic researcher from Howard University. The author has contributed to research in topics: Promoter & Gene. The author has an hindex of 7, co-authored 7 publications receiving 487 citations.
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Epigenetics across the human lifespan
TL;DR: This review describes the various types of endogenous human developmental milestones such as birth, puberty, and menopause, as well as the diverse exogenous environmental factors that influence human health, in a chronological epigenetic context and presents a comprehensive new hypothesis of how these diverse environmental factors cause both direct and indirect epigenetic changes.
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Cellular Senescence as the Causal Nexus of Aging
TL;DR: This paper proposes that cellular senescence is the ultimate driver of the aging process, as a “causal nexus” that bridges microscopic subcellular damage with the phenotypic, macroscopic effect of aging.
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Cellular reprogramming for understanding and treating human disease.
TL;DR: It is shown how stem cells can be used to create in vitro models of human disease and examples of how reprogramming is being used to study and treat such diverse diseases as cancer, aging, and accelerated aging syndromes, infectious diseases such as AIDS, and epigenetic diseasessuch as polycystic ovary syndrome.
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Epigenetic Mechanisms of Integrative Medicine
Riya R. Kanherkar,Susan E. Stair,Naina Bhatia-Dey,Paul J. Mills,Deepak Chopra,Antonei B. Csoka +5 more
TL;DR: IM's ability to affect healing is due at least in part to epigenetic mechanisms, and emphasis on mapping, deciphering, and optimizing these effects will facilitate therapeutic delivery and create further benefits.
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Pro-fibrotic pathway activation in trabecular meshwork and lamina cribrosa is the main driving force of glaucoma
Alex Zhavoronkov,Evgeny Izumchenko,Riya R. Kanherkar,Mahder Teka,Charles R. Cantor,Kebreten F. Manaye,David Sidransky,Michael D. West,Eugene Makarev,Antonei B. Csoka +9 more
TL;DR: Applying a pathway analysis algorithm, it is discovered that an elevated level of TGFβ observed in glaucoma-affected tissues could lead to pro-fibrotic pathway activation in TM and in LC, making TM less efficient in AH drainage and making LC more susceptible to damage from elevated IOP via ECM transformation in LC.