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Article ; Online: Tackling Counterfeit Drugs: The Challenges and Possibilities.

Pathak, Ranjana / Gaur, Vaibhav / Sankrityayan, Himanshu / Gogtay, Jaideep

2023 Volume 37, Issue 4, Page(s) 281–290

Abstract: Drugs that have been manufactured or packaged fraudulently are referred to as counterfeit/fake/spurious/falsified drugs because they either lack active ingredients or have the incorrect dosages. Counterfeiting of drugs has become a global issue with ... ...

Abstract	Drugs that have been manufactured or packaged fraudulently are referred to as counterfeit/fake/spurious/falsified drugs because they either lack active ingredients or have the incorrect dosages. Counterfeiting of drugs has become a global issue with which the whole world is grappling. The World Health Organization states the frightening figure in which almost 10.5% of the medications worldwide are either subpar or fake. Although developing and low-income countries are the targets of the large-scale drug counterfeiting activities, fake/substandard drugs are also making their way into developed nations including the USA, Canada, and European countries. Counterfeiting of drugs is leading to not only economic loss but is also playing its part in the morbidity and mortality of patients. The recent COVID-19 pandemic fuelled the demand for certain categories of medicines such as antipyretics, remdesivir, corticosteroids, vaccines, etc., thus increasing the demand and manufacture of subpar/fake medicines. This review articulates the current trends and global impact of drug counterfeiting, current and potential measures for its prevention and the role of different stakeholders in tackling the menace of drug counterfeiting.
MeSH term(s)	Humans ; Developing Countries ; Counterfeit Drugs ; Pandemics ; COVID-19/prevention & control ; World Health Organization
Chemical Substances	Counterfeit Drugs
Language	English
Publishing date	2023-05-15
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2415165-8
ISSN	1179-1993 ; 1178-2595
ISSN (online)	1179-1993
ISSN	1178-2595
DOI	10.1007/s40290-023-00468-w
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Zs.A 2034: Show issues

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Article ; Online: Evaluating the potential of tauroursodeoxycholic acid as add-on therapy in amelioration of streptozotocin-induced diabetic kidney disease.

Sankrityayan, Himanshu / Shelke, Vishwadeep / Kale, Ajinath / Gaikwad, Anil Bhanudas

European journal of pharmacology

2023 Volume 942, Page(s) 175528

Abstract: The bile acid tauroursodeoxycholic acid (TUDCA) is of natural origin and is used in traditional Chinese medicine for centuries. Earlier its use was limited to biliary disorders but owing to its pleiotropic effects dietary TUDCA supplementation is under ... ...

Abstract	The bile acid tauroursodeoxycholic acid (TUDCA) is of natural origin and is used in traditional Chinese medicine for centuries. Earlier its use was limited to biliary disorders but owing to its pleiotropic effects dietary TUDCA supplementation is under clinical trials for diseases including type 1 and 2 diabetic complications. The current study aims to evaluate the potential and underlying molecular mechanism of the TUDCA as a monotherapy and as an add-on therapy to telmisartan, an angiotensin II type 1 receptor (AT1R) blocker against diabetic kidney disease (DKD). We employed both in-vitro and in-vivo approaches where NRK-52E cells were incubated with high glucose, and DKD was induced in Wistar rats using streptozotocin (55 mg/kg, i.p.). After 4 weeks, animals were administered with TUDCA (250 mg/kg, i.p.), telmisartan (10 mg/kg, p.o.), and their combination for 4 weeks. Plasma was collected for the biochemical estimation and kidneys were used for immunoblotting, PCR, and histopathological analysis. Similarly, for in-vitro experiments, cells were exposed to 1000 μM of TUDCA and 10 μM of telmisartan, and their combination, followed by cell lysate collection and immunoblotting analysis. We observed that the addition of TUDCA to conventional telmisartan treatment was more effective in restoring the renal function decline and suppressing the apoptotic and fibrotic signaling as compared to monotherapies of AT1R blocker and ER stress inhibitor. The results implicate the utility of traditionally used TUDCA as a potential renoprotective compound. Since, both TUDCA and telmisartan are approved for clinical usage, thus concomitant administration of them could be a novel therapeutic strategy against DKD.
MeSH term(s)	Rats ; Animals ; Diabetic Nephropathies/drug therapy ; Telmisartan/pharmacology ; Telmisartan/therapeutic use ; Streptozocin ; Rats, Wistar ; Taurochenodeoxycholic Acid/pharmacology ; Taurochenodeoxycholic Acid/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/pharmacology ; Angiotensin II Type 1 Receptor Blockers/therapeutic use ; Diabetes Mellitus/drug therapy
Chemical Substances	ursodoxicoltaurine (60EUX8MN5X) ; Telmisartan (U5SYW473RQ) ; Streptozocin (5W494URQ81) ; Taurochenodeoxycholic Acid (516-35-8) ; Angiotensin II Type 1 Receptor Blockers
Language	English
Publishing date	2023-01-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2023.175528
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Article ; Online: Cyproheptadine, a SET7/9 inhibitor, reduces hyperglycaemia-induced ER stress alleviating inflammation and fibrosis in renal tubular epithelial cells.

Sankrityayan, Himanshu / Kale, Ajinath / Shelke, Vishwadeep / Gaikwad, Anil Bhanudas

Archives of physiology and biochemistry

2022 , Page(s) 1–9

Abstract: Context: Persistent hyperglycaemia increases SET7/9 expression and endoplasmic reticulum (ER) stress which causes inflammation, apoptosis, and fibrosis in renal tubular epithelial cells leading to diabetic kidney disease (DKD).: Objective: Current ... ...

Abstract	Context: Persistent hyperglycaemia increases SET7/9 expression and endoplasmic reticulum (ER) stress which causes inflammation, apoptosis, and fibrosis in renal tubular epithelial cells leading to diabetic kidney disease (DKD). Objective: Current study explores the renoprotective potential of a novel SET7/9 inhibitor, Cyproheptadine, and the underlying molecular mechanisms in hyperglycaemia-induced renal tubular epithelial cell injury. Methods: Change in expression of SET7/9, histone H3 lysine (K4) monomethylation (H3K4Me1), inflammatory, fibrotic, and ER stress proteins were evaluated Results: SET7/9 and H3K4Me1 expression significantly increased with ER stress, inflammation, apoptosis, and fibrosis, Conclusion: Cyproheptadine prevented hyperglycaemia-induced renal fibrosis and inflammation by reducing H3K4Me1 expression and ER stress.
Language	English
Publishing date	2022-08-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1238320-x
ISSN	1744-4160 ; 1381-3455
ISSN (online)	1744-4160
ISSN	1381-3455
DOI	10.1080/13813455.2022.2105365
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Article ; Online: Inhibition of endoplasmic reticulum stress combined with activation of angiotensin-converting enzyme 2: novel approach for the prevention of endothelial dysfunction in type 1 diabetic rats.

Sankrityayan, Himanshu / Kale, Ajinath / Gaikwad, Anil Bhanudas

Canadian journal of physiology and pharmacology

2021 Volume 100, Issue 3, Page(s) 234–239

Abstract: Persistent hyperglycemia in type 1 diabetes triggers numerous signaling pathways, which may prove deleterious to the endothelium. As hyperglycemia damages the endothelial layer via multiple signaling pathways, including enhanced oxidative stress, ... ...

Abstract	Persistent hyperglycemia in type 1 diabetes triggers numerous signaling pathways, which may prove deleterious to the endothelium. As hyperglycemia damages the endothelial layer via multiple signaling pathways, including enhanced oxidative stress, downregulation of angiotensin-converting enzyme 2 signaling, and exacerbation of endoplasmic reticulum (ER) stress, it becomes difficult to prevent injury using monotherapy. Thus, the present study was conceived to evaluate the combined effect of ER stress inhibition along with angiotensin-converting enzyme 2 activation, two major contributors to hyperglycemia-induced endothelial dysfunction, in preventing endothelial dysfunction associated with type 1 diabetes. Streptozotocin-induced diabetic animals were treated with either diminazene aceturate (5 mg·kg
MeSH term(s)	Angiotensin-Converting Enzyme 2/metabolism ; Animals ; Diabetes Mellitus, Experimental ; Diabetes Mellitus, Type 1/drug therapy ; Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/physiopathology ; Diminazene/administration & dosage ; Diminazene/analogs & derivatives ; Diminazene/pharmacology ; Drug Therapy, Combination ; Endoplasmic Reticulum Stress/drug effects ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiopathology ; Male ; Oxidative Stress/drug effects ; Rats, Wistar ; Streptozocin ; Taurochenodeoxycholic Acid/administration & dosage ; Taurochenodeoxycholic Acid/pharmacology ; Rats
Chemical Substances	Taurochenodeoxycholic Acid (516-35-8) ; Streptozocin (5W494URQ81) ; ursodoxicoltaurine (60EUX8MN5X) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; diminazene aceturate (JI8SAD85NO) ; Diminazene (Y5G36EEA5Z)
Language	English
Publishing date	2021-09-29
Publishing country	Canada
Document type	Journal Article
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/cjpp-2021-0170
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Zs.A 589: Show issues

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Article ; Online: Epigenetic restoration of endogenous Klotho expression alleviates acute kidney injury-diabetes comorbidity.

Kale, Ajinath / Sankrityayan, Himanshu / Gaikwad, Anil Bhanudas

Life sciences

2021 Volume 288, Page(s) 120194

Abstract: Aims: The present study aimed at exploring the mechanisms behind Klotho regulation in hyperglycemia augmented AKI. In addition, epigenetic ways to restore the Klotho expression in AKI-diabetes comorbidity have been evaluated.: Main methods: Bilateral ...

Abstract	Aims: The present study aimed at exploring the mechanisms behind Klotho regulation in hyperglycemia augmented AKI. In addition, epigenetic ways to restore the Klotho expression in AKI-diabetes comorbidity have been evaluated. Main methods: Bilateral ischemia-reperfusion injury (IRI) and chemical hypoxia-reperfusion injury (HRI) were developed in diabetic rats and, NRK52E cells under high glucose conditions respectively, to mimic the AKI condition. Plasma, urine, tubular lysate of the kidney and NRK52E cell lysate were used for biochemical, ELISA, histology, immunoblotting, RT-PCR and RNA interference studies. Key findings: Hyperglycemia significantly aggravated IRI/HRI induced AKI as evidenced by biochemical and histological results. We also observed a significant increase in expressions of kidney specific histone deacetylases (HDACs), apoptotic and inflammatory proteins, and decrease in levels of endogenous Klotho, H3K9Ac and H3K27Ac proteins in hyperglycemic IRI/HRI groups. Significance: Diabetes comorbidity exaggerates AKI, where endogenous Klotho loss could be a potential connecting link. However, kidney-specific HDACs inhibition showed reno-protection via restoring the endogenous Klotho loss and thus prevention of inflammation and apoptosis, which could prove to be a potential therapeutic strategy against diabetes-AKI comorbidity.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/prevention & control ; Animals ; Diabetes Mellitus, Experimental/complications ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Diabetic Nephropathies/prevention & control ; Gene Expression Regulation/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Klotho Proteins/genetics ; Klotho Proteins/metabolism ; Male ; Rats ; Rats, Wistar
Chemical Substances	Histone Deacetylase Inhibitors ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2021-12-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120194
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Article: Epigenetic restoration of endogenous Klotho expression alleviates acute kidney injury-diabetes comorbidity

Kale, Ajinath / Sankrityayan, Himanshu / Gaikwad, Anil Bhanudas

Life sciences. 2022 Jan. 01, v. 288

2022

Abstract: The present study aimed at exploring the mechanisms behind Klotho regulation in hyperglycemia augmented AKI. In addition, epigenetic ways to restore the Klotho expression in AKI-diabetes comorbidity have been evaluated.Bilateral ischemia-reperfusion ... ...

Abstract	The present study aimed at exploring the mechanisms behind Klotho regulation in hyperglycemia augmented AKI. In addition, epigenetic ways to restore the Klotho expression in AKI-diabetes comorbidity have been evaluated.Bilateral ischemia-reperfusion injury (IRI) and chemical hypoxia-reperfusion injury (HRI) were developed in diabetic rats and, NRK52E cells under high glucose conditions respectively, to mimic the AKI condition. Plasma, urine, tubular lysate of the kidney and NRK52E cell lysate were used for biochemical, ELISA, histology, immunoblotting, RT-PCR and RNA interference studies.Hyperglycemia significantly aggravated IRI/HRI induced AKI as evidenced by biochemical and histological results. We also observed a significant increase in expressions of kidney specific histone deacetylases (HDACs), apoptotic and inflammatory proteins, and decrease in levels of endogenous Klotho, H3K9Ac and H3K27Ac proteins in hyperglycemic IRI/HRI groups.Diabetes comorbidity exaggerates AKI, where endogenous Klotho loss could be a potential connecting link. However, kidney-specific HDACs inhibition showed reno-protection via restoring the endogenous Klotho loss and thus prevention of inflammation and apoptosis, which could prove to be a potential therapeutic strategy against diabetes-AKI comorbidity.
Keywords	RNA interference ; apoptosis ; comorbidity ; epigenetics ; glucose ; histology ; histone deacetylase ; hyperglycemia ; immunoblotting ; inflammation ; kidneys ; therapeutics ; urine
Language	English
Dates of publication	2022-0101
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120194
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Article ; Online: Long non-coding RNAs as emerging regulators of miRNAs and epigenetics in diabetes-related chronic kidney disease.

Shelke, Vishwadeep / Kale, Ajinath / Sankrityayan, Himanshu / Anders, Hans-Joachim / Gaikwad, Anil Bhanudas

Archives of physiology and biochemistry

2022 Volume 130, Issue 2, Page(s) 230–241

Abstract: Diabetes is one of the major cause of chronic kidney disease (CKD), including "diabetic nephropathy," and is an increasingly prevalent accelerator of the progression of non-diabetic forms of CKD. The long non-coding RNAs (lncRNAs) have come into the ... ...

Abstract	Diabetes is one of the major cause of chronic kidney disease (CKD), including "diabetic nephropathy," and is an increasingly prevalent accelerator of the progression of non-diabetic forms of CKD. The long non-coding RNAs (lncRNAs) have come into the limelight in the past few years as one of the emerging weapons against CKD in diabetes. Available data over the past few years demonstrate the interaction of lncRNAs with miRNAs and epigenetic machinery. Interestingly, the evolving data suggest that lncRNAs play a vital role in diabetes-associated CKD by regulation of epigenetic enzymes such as DNA methyltransferase, histone deacetylases, and histone methyltransferases. LncRNAs are also engaged in the regulation of several miRNAs in diabetic nephropathy. Hence this review will elaborate on the association between lncRNAs and their interaction with epigenetic regulators involved in different aspects and thus the progression of CKD in diabetes.
MeSH term(s)	Humans ; MicroRNAs/genetics ; RNA, Long Noncoding/genetics ; Diabetic Nephropathies/genetics ; Epigenesis, Genetic ; Renal Insufficiency, Chronic/genetics ; Diabetes Mellitus/genetics
Chemical Substances	MicroRNAs ; RNA, Long Noncoding
Language	English
Publishing date	2022-01-05
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	1238320-x
ISSN	1744-4160 ; 1381-3455
ISSN (online)	1744-4160
ISSN	1381-3455
DOI	10.1080/13813455.2021.2023580
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Article ; Online: Klotho: A possible mechanism of action of SGLT2 inhibitors preventing episodes of acute kidney injury and cardiorenal complications of diabetes.

Kale, Ajinath / Sankrityayan, Himanshu / Anders, Hans-Joachim / Bhanudas Gaikwad, Anil

Drug discovery today

2021 Volume 26, Issue 8, Page(s) 1963–1971

Abstract: Diabetes and cardiorenal comorbidities are major global health concerns, with high economic burdens and mortality rates. Sodium glucose co-transporter-2 inhibitors (SGLT2is) are novel US Food and Drug Administration (FDA)-approved antihyperglycemics with ...

Abstract	Diabetes and cardiorenal comorbidities are major global health concerns, with high economic burdens and mortality rates. Sodium glucose co-transporter-2 inhibitors (SGLT2is) are novel US Food and Drug Administration (FDA)-approved antihyperglycemics with unexpected protective potential against cardiorenal diseases in patients with or without type 2 diabetes mellitus (T2DM). Despite initial concerns, the incidence of episodes of acute kidney injury (AKI) was significantly lower in patients taking SGLT2i compared with other therapies or placebo. Evolving data suggest a link between SGLT2is and the anti-aging protein Klotho in the amelioration of diabetes and cardiorenal diseases. Here, we consider Klotho and SGLT2is as a novel therapeutic approach for the management of AKI and other cardiorenal complications in patients with or without diabetes.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/prevention & control ; Animals ; Diabetic Cardiomyopathies/prevention & control ; Diabetic Nephropathies/prevention & control ; Humans ; Hypoglycemic Agents/pharmacology ; Klotho Proteins/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology
Chemical Substances	Hypoglycemic Agents ; Sodium-Glucose Transporter 2 Inhibitors ; KL protein, human (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2021-04-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2021.04.007
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Article ; Online: Endoplasmic Reticulum Stress and Renin-Angiotensin System Crosstalk in Endothelial Dysfunction.

Sankrityayan, Himanshu / Rao, Pooja Dhileepkumar / Shelke, Vishwadeep / Kulkarni, Yogesh A / Mulay, Shrikant R / Gaikwad, Anil Bhanudas

Current molecular pharmacology

2022 Volume 16, Issue 2, Page(s) 139–146

Abstract: Background: Vascular endothelial dysfunction (VED) significantly results in catastrophic cardiovascular diseases with multiple aetiologies. Variations in vasoactive peptides, including angiotensin II and endothelin 1, and metabolic perturbations like ... ...

Abstract	Background: Vascular endothelial dysfunction (VED) significantly results in catastrophic cardiovascular diseases with multiple aetiologies. Variations in vasoactive peptides, including angiotensin II and endothelin 1, and metabolic perturbations like hyperglycaemia, altered insulin signalling, and homocysteine levels result in pathogenic signalling cascades, which ultimately lead to VED. Endoplasmic reticulum (ER) stress reduces nitric oxide availability, causes aberrant angiogenesis, and enhances oxidative stress pathways, consequently promoting endothelial dysfunction. Moreover, the renin-angiotensin system (RAS) has widely been acknowledged to impact angiogenesis, endothelial repair and inflammation. Interestingly, experimental studies at the preclinical level indicate a possible pathological link between the two pathways in the development of VED. Furthermore, pharmacological modulation of ER stress ameliorates angiotensin-II mediated VED as well as RAS intervention either through inhibition of the pressor arm or enhancement of the depressor arm of RAS, mitigating ER stress-induced endothelial dysfunction and thus emphasizing a vital crosstalk. Conclusion: Deciphering the pathway overlap between RAS and ER stress may open potential therapeutic avenues to combat endothelial dysfunction and associated diseases. Several studies suggest that alteration in a component of RAS may induce ER stress or induction of ER stress may modulate the RAS components. In this review, we intend to elaborate on the crosstalk of ER stress and RAS in the pathophysiology of VED.
MeSH term(s)	Humans ; Angiotensin II/pharmacology ; Endoplasmic Reticulum Stress/physiology ; Endothelium, Vascular/metabolism ; Renin-Angiotensin System ; Vascular Diseases/metabolism
Chemical Substances	Angiotensin II (11128-99-7)
Language	English
Publishing date	2022-12-05
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1874-4702
ISSN (online)	1874-4702
DOI	10.2174/1874467215666220301113833
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Article ; Online: Klotho in kidney diseases: a crosstalk between the renin-angiotensin system and endoplasmic reticulum stress.

Kale, Ajinath / Sankrityayan, Himanshu / Anders, Hans-Joachim / Gaikwad, Anil Bhanudas

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2021 Volume 38, Issue 4, Page(s) 819–825

Abstract: Klotho is a transmembrane anti-ageing protein that exists in three forms, i.e. α-Klotho, β-Klotho and γ-Klotho, with distinct organ-specific expression and functions in the body. Here we focus on α-Klotho (hereafter Klotho), abundantly expressed by the ... ...

Abstract	Klotho is a transmembrane anti-ageing protein that exists in three forms, i.e. α-Klotho, β-Klotho and γ-Klotho, with distinct organ-specific expression and functions in the body. Here we focus on α-Klotho (hereafter Klotho), abundantly expressed by the distal and proximal convoluted tubules of the kidney. A significant decline in systemic and renal Klotho levels is a new hallmark for kidney disease progression. Emerging research portrays Klotho as a promising diagnostic and therapeutic target for diabetic and non-diabetic kidney disease. Even so, the underlying mechanisms of Klotho regulation and the strategies to restore its systemic and renal levels are still lacking. Angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers are the current standard of care for kidney diseases, but the molecular mechanisms for their nephroprotective action are still ambiguous. Moreover, endoplasmic reticulum (ER) stress also plays a crucial role in kidney disease progression. Few studies have claimed that the renin-angiotensin-aldosterone system (RAAS) has a direct relation with ER stress generation and vice versa in kidney disease. Interestingly, RAAS and ER stress modulation are associated with Klotho regulation in kidney disease. Here we focus on how the RAAS and ER stress connect with Klotho regulation in kidney disease. We also discuss Klotho and ER stress in an alliance with the concept of haemodynamic and metabolic overload in kidney disease. In addition, we highlight novel approaches to implement Klotho as a therapeutic target via RAAS and ER stress modulation for the treatment of diabetic and non-diabetic kidney diseases.
MeSH term(s)	Humans ; Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Disease Progression ; Endoplasmic Reticulum Stress ; Kidney Diseases/drug therapy ; Renin-Angiotensin System/physiology ; Klotho Proteins/metabolism
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2021-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfab340
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