TY - JOUR
T1 - Molecular prospect of type-2 diabetes
T2 - Nanotechnology based diagnostics and therapeutic intervention
AU - Kerry, Rout George
AU - Mahapatra, Gyana Prakash
AU - Maurya, Ganesh Kumar
AU - Patra, Sushmita
AU - Mahari, Subhasis
AU - Das, Gitishree
AU - Patra, Jayanta Kumar
AU - Sahoo, Sabuj
N1 - Publisher Copyright:
© 2020, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2021/6
Y1 - 2021/6
N2 - About ninety percent of all diabetic conditions account for T2D caused due to abnormal insulin secretion/ action or increased hepatic glucose production. Factors that contribute towards the aetiology of T2D could be well explained through biochemical, molecular, and cellular aspects. In this review, we attempt to explain the recent evolving molecular and cellular advancement associated with T2D pathophysiology. Current progress fabricated in T2D research concerning intracellular signaling cascade, inflammasome, autophagy, genetic and epigenetics changes is discretely explained in simple terms. Present available anti-diabetic therapeutic strategies commercialized and their limitations which are needed to be acknowledged are addressed in the current review. In particular, the pre-eminence of nanotechnology-based approaches to nullify the inadequacy of conventional anti-diabetic therapeutics and heterogeneous nanoparticulated systems exploited in diabetic researches are also discretely mentioned and are also listed in a tabular format in the review. Additionally, as a future prospect of nanotechnology, the review presents several strategic hypotheses to ameliorate the austerity of T2D by an engineered smart targeted nano-delivery system. In detail, an effort has been made to hypothesize novel nanotechnological based therapeutic strategies, which exploits previously described inflammasome, autophagic target points. Utilizing graphical description it is explained how a smart targeted nano-delivery system could promote β-cell growth and development by inducing the Wnt signaling pathway (inhibiting Gsk3β), inhibiting inflammasome (inhibiting NLRP3), and activating autophagic target points (protecting Atg3/Atg7 complex from oxidative stress) thereby might ameliorate the severity of T2D. Additionally, several targeting molecules associated with autophagic and epigenetic factors are also highlighted, which can be exploited in future diabetic research.
AB - About ninety percent of all diabetic conditions account for T2D caused due to abnormal insulin secretion/ action or increased hepatic glucose production. Factors that contribute towards the aetiology of T2D could be well explained through biochemical, molecular, and cellular aspects. In this review, we attempt to explain the recent evolving molecular and cellular advancement associated with T2D pathophysiology. Current progress fabricated in T2D research concerning intracellular signaling cascade, inflammasome, autophagy, genetic and epigenetics changes is discretely explained in simple terms. Present available anti-diabetic therapeutic strategies commercialized and their limitations which are needed to be acknowledged are addressed in the current review. In particular, the pre-eminence of nanotechnology-based approaches to nullify the inadequacy of conventional anti-diabetic therapeutics and heterogeneous nanoparticulated systems exploited in diabetic researches are also discretely mentioned and are also listed in a tabular format in the review. Additionally, as a future prospect of nanotechnology, the review presents several strategic hypotheses to ameliorate the austerity of T2D by an engineered smart targeted nano-delivery system. In detail, an effort has been made to hypothesize novel nanotechnological based therapeutic strategies, which exploits previously described inflammasome, autophagic target points. Utilizing graphical description it is explained how a smart targeted nano-delivery system could promote β-cell growth and development by inducing the Wnt signaling pathway (inhibiting Gsk3β), inhibiting inflammasome (inhibiting NLRP3), and activating autophagic target points (protecting Atg3/Atg7 complex from oxidative stress) thereby might ameliorate the severity of T2D. Additionally, several targeting molecules associated with autophagic and epigenetic factors are also highlighted, which can be exploited in future diabetic research.
KW - Autophagy
KW - Epigenetics
KW - Inflammasome
KW - Intracellular signaling cascade
KW - Nano-delivery systems
KW - Type-2 diabetes
UR - http://www.scopus.com/inward/record.url?scp=85092582833&partnerID=8YFLogxK
U2 - 10.1007/s11154-020-09606-0
DO - 10.1007/s11154-020-09606-0
M3 - Review article
C2 - 33052523
AN - SCOPUS:85092582833
SN - 1389-9155
VL - 22
SP - 421
EP - 451
JO - Reviews in Endocrine and Metabolic Disorders
JF - Reviews in Endocrine and Metabolic Disorders
IS - 2
ER -
