LVKS Bhaskar

Dr. LVKS Bhaskar

orcid

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2021 in Journal of Drug Delivery Science and Technology
Verified
Journal Article
Closed access
TSTarun Sahu
Tarun Sahu
YRYashwant Kumar Ratre
Yashwant Kumar Ratre
SCSushma Chauhan
Sushma Chauhan
LBLVKS Bhaskar
LVKS Bhaskar
MNMaya P. Nair
Maya P. Nair
HVHenu Kumar Verma
Henu Kumar Verma

3 May 2023 in Biomedicine & Pharmacotherapy
Verified
Journal Article
Open access
EPEluri Pavitra
Eluri Pavitra
JKJyothsna Kancharla
Jyothsna Kancharla
VGVivek Kumar Gupta
Vivek Kumar Gupta
KPKiran Prasad
Kiran Prasad
JSJu Yong Sung
Ju Yong Sung
YHYun Suk Huh
Yun Suk Huh
Breast cancer (BC) is the second most fatal disease and is the prime cause of cancer allied female deaths. BC is caused by aberrant tumor suppressor genes and oncogenes regulated by transcription factors (TFs) like NF-κB. NF-κB is a pro-inflammatory TF that crucially alters the expressions of various genes associated with inflammation, cell progression, metastasis, and apoptosis and modulates a network of genes that underlie tumorigenesis. Herein, we focus on NF-κB signaling pathways, its regulators, and the rationale for targeting NF-κB. This review also includes TFs that maintain NF-κB crosstalk and their roles in promoting angiogenesis and metastasis. In addition, we discuss the importance of combination therapies, resistance to treatment, and potential novel therapeutic strategies including nanomedicine that targets NF-κB.

11 January 2016 in Journal of Biomedical Science
Verified
Journal Article
Open access
PDF file
GRGnanasambandan Ramanathan
Gnanasambandan Ramanathan
RERamprasad Elumalai
Ramprasad Elumalai
SPSoundararajan Periyasamy
Soundararajan Periyasamy
LBLVKS Bhaskar
LVKS Bhaskar
Autosomal dominant polycystic kidney disease (ADPKD) is a monogenic disorder and is a common genetic cause of chronic renal failure in children and adults. The enzyme renin plays a key role in the RAAS cascade and an important role in the development of hypertension and progression of renal disease in ADPKD. The present study is aimed to investigate the potential modifier effect of REN gene polymorphisms on the progression of chronic kidney disease (CKD) in ADPKD. We analyzed 102 ADPKD patients and 106 healthy controls from the same geographic area. FRET-based KASPar single-nucleotide polymorphism (SNP) genotyping assays for REN gene tag-SNPs (rs2887284, rs2368564, rs1464816, rs7521667, rs10900555, rs6693954, rs6676670 and rs11571078) were performed. Cochran-Armitage trend test was used to assess the potential associations between these polymorphisms and CKD stages. Haplotype frequencies and LD measures were estimated by using the software Haploview. Mantel-Haenszel stratified analysis was used to explore confounding and interaction effects of these polymorphisms. Of the eight tag-SNPs genotyped, the rs10900555 polymorphism deviated from the Hardy-Weinberg equilibrium in controls. The presence of ADPKD in general was not significantly associated with the REN tag-SNPs included in this study. Linkage disequilibrium analysis yielded three haplotype blocks and the haplotypes of the respective blocks are not statistically different between ADPKD and controls. In multivariate analysis, the rs1464816 TG genotype showed a significant association with the advancement of CKD in ADPKD (OR = 4.80; 95 % CI = 1.30–17.82; p = 0.019). The present study provides evidence that the rs1464816 polymorphism in REN is associated with CKD progression in ADPKD.

8 October 2021 in Frontiers in Physiology
Verified
Journal Article
Open access
TSTianyi Shao
Tianyi Shao
HVHenu Kumar Verma
Henu Kumar Verma
BPBabita Pande
Babita Pande
VCVincenzo Costanzo
Vincenzo Costanzo
Weibing YeWeibing Ye
Weibing Ye
LBLVKS Bhaskar
LVKS Bhaskar
Physical activity (PA) and nutrition are the essential components of a healthy lifestyle, as they can influence energy balance, promote functional ability of various systems and improve immunity. Infections and their associated symptoms are the common and frequent challenges to human health that are causing severe economic and social consequences around the world. During aging, human immune system undergoes dramatic aging-related changes/dysfunctions known as immunosenescence. Clinically, immunosenescence refers to the gradual deterioration of immune system that increases exposure to infections, and reduces vaccine efficacy. Such phenomenon is linked to impaired immune responses that lead to dysfunction of multiple organs, while lack of physical activity, progressive loss of muscle mass, and concomitant decline in muscle strength facilitate immunosenescence and inflammation. In the present review, we have discussed the role of nutrition and PA, which can boost the immune system alone and synergistically. Evidence suggests that long-term PA is beneficial in improving immune system and preventing various infections. We have further discussed several nutritional strategies for improving the immune system. Unfortunately, the available evidence shows conflicting results. In terms of interaction with food intake, PA does not tend to increase energy intake during a short time course. However, overcoming nutritional deficiencies appears to be the most practical recommendation. Through the balanced nutritious diet intake one can fulfill the bodily requirement of optimal nutrition that significantly impacts the immune system. Supplementation of a single nutrient as food is generally not advisable. Rather incorporating various fruits and vegetables, whole grains, proteins and probiotics may ensure adequate nutrient intake. Therefore, multi-nutrient supplements may benefit people having deficiency in spite of sufficient diet. Along with PA, supplementation of probiotics, bovine colostrum, plant-derived products and functional foods may provide additional benefits in improving the immune system.

1 February 2021 in Seminars in Cancer Biology
Verified
Journal Article
Closed access
EPEluri Pavitra
Eluri Pavitra
BDBegum Dariya
Begum Dariya
GSGowru Srivani
Gowru Srivani
SKSung-Min Kang
Sung-Min Kang
AAAfroz Alam
Afroz Alam
YHYun Suk Huh
Yun Suk Huh

1 January 2022 in Oxidative Medicine and Cellular Longevity
Verified
Journal Article
Open access
PDF file
PPPoojarani Panda
Poojarani Panda
HVHenu Kumar Verma
Henu Kumar Verma
SLSaikrishna Lakkakula
Saikrishna Lakkakula
NMNeha Merchant
Neha Merchant
FKFairrul Kadir
Fairrul Kadir
VISWESWARA RAO PASUPULETIVISWESWARA RAO PASUPULETI
VISWESWARA RAO PASUPULETI
Cardiovascular disease (CVD) is a broad term that incorporated a group of conditions that affect the blood vessels and the heart. CVD is a foremost cause of fatalities around the world. Multiple pathophysiological mechanisms are involved in CVD; however, oxidative stress plays a vital role in generating reactive oxygen species (ROS). Oxidative stress occurs when the concentration of oxidants exceeds the potency of antioxidants within the body while producing reactive nitrogen species (RNS). ROS generated by oxidative stress disrupts cell signaling, DNA damage, lipids, and proteins, thereby resulting in inflammation and apoptosis. Mitochondria is the primary source of ROS production within cells. Increased ROS production reduces nitric oxide (NO) bioavailability, which elevates vasoconstriction within the arteries and contributes to the development of hypertension. ROS production has also been linked to the development of atherosclerotic plaque. Antioxidants can decrease oxidative stress in the body; however, various therapeutic drugs have been designed to treat oxidative stress damage due to CVD. The present review provides a detailed narrative of the oxidative stress and ROS generation with a primary focus on the oxidative stress biomarker and its association with CVD. We have also discussed the complex relationship between inflammation and endothelial dysfunction in CVD as well as oxidative stress‐induced obesity in CVD. Finally, we discussed the role of antioxidants in reducing oxidative stress in CVD.