Treatment with high dose salicylates improves cardiometabolic parameters: Meta-analysis of randomized controlled trials

Baye, Estifanos; Naderpoor, Negar; Misso, Marie; Teede, Helena; Moran, Lisa J.; Courten, Barbora de

doi:10.1016/j.metabol.2017.03.006

Cited by 4 publications

(3 citation statements)

References 57 publications

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“… 80 Recent studies have shown that salicylates have anti-inflammatory effects that involve inhibition of NF-κB and that they also prevent diabetes and improve insulin resistance in experimental models and humans. 81 , 82 Drugs such as glicazide and troglitazone, as well as N-acetylcysteine, decrease inflammatory markers in patients with diabetic nephropathy and diabetic retinopathy. 83 …”

Section: Mechanisms Of Vascular Complications In Diabetes and The Impmentioning

confidence: 99%

Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms

Petrie

Guzik

Touyz

2018

Canadian Journal of Cardiology

1,231

779

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Hypertension and type 2 diabetes are common comorbidities. Hypertension is twice as frequent in patients with diabetes compared with those who do not have diabetes. Moreover, patients with hypertension often exhibit insulin resistance and are at greater risk of diabetes developing than are normotensive individuals. The major cause of morbidity and mortality in diabetes is cardiovascular disease, which is exacerbated by hypertension. Accordingly, diabetes and hypertension are closely interlinked because of similar risk factors, such as endothelial dysfunction, vascular inflammation, arterial remodelling, atherosclerosis, dyslipidemia, and obesity. There is also substantial overlap in the cardiovascular complications of diabetes and hypertension related primarily to microvascular and macrovascular disease. Common mechanisms, such as upregulation of the renin-angiotensin-aldosterone system, oxidative stress, inflammation, and activation of the immune system likely contribute to the close relationship between diabetes and hypertension. In this article we discuss diabetes and hypertension as comorbidities and discuss the pathophysiological features of vascular complications associated with these conditions. We also highlight some vascular mechanisms that predispose to both conditions, focusing on advanced glycation end products, oxidative stress, inflammation, the immune system, and microRNAs. Finally, we provide some insights into current therapies targeting diabetes and cardiovascular complications and introduce some new agents that may have vasoprotective therapeutic potential in diabetes.

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Section: Mechanisms Of Vascular Complications In Diabetes and The Impmentioning

confidence: 99%

Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms

Petrie

Guzik

Touyz

2018

Canadian Journal of Cardiology

1,231

779

View full text Add to dashboard Cite

show abstract

“…Nuclear factor-kappa B (NF- κ B) has been pointed out to play important parts in the inflammatory process linking chronic inflammation and cancer, its activation participating in all known cancer hallmarks, including enhanced proliferation and survival, stemness acquisition of cancer cells, promoted genetic and epigenetic alterations, drug resistance, and immune suppression 239 . Meanwhile, suppression of NF- κ B showed preventive effects on diabetes development and insulin resistance, cardiovascular events, which are genetically related to diabetes, chemotherapy-induced neuropathic pain, CVD, and other adverse effects 240 , 241 , 242 , 243 . Hence, the extensive involvement in cancer and cancer-related undesirable effects renders this transcriptional factor an appealing therapeutic target to free two birds with one key.…”

Section: Lessons To Learn From Cancer Complications and Comorbiditiesmentioning

confidence: 99%

“… Shared mechanism Basic science evidence Potential one-key-two-birds target Ref. Chronic inflammation ↑ Cancer development across all stages of tumorigenesis ↑ CVD, COPD, diabetes, and neurodegenerative disorders IL-1 β , IL-6, TNF- α , NF- κ B, and PPAR γ 137 , 238 , 239 , 240 , 241 , 242 , 243 , 244 , 247 , 248 Oxidative stress ↑ The initiation and progression of cancer ↑ The pathogenesis of CVD, pulmonary diseases, diabetes, infections, and neurodegenerative disorders HO1, catalase, SOD, GPX, NF- κ B, Nrf2, TGF- β , TNF- α , and PPAR γ 249 , 252 , 255 , 258 , 259 , 260 , 261 , 262 , 263 , 264 , 265 , 266 Angiogenesis ↑Tumor progression with independent blood supply ↑ CVD, pulmonary hypertension, diabetic retinopathy, obesity, diabetes, neurodegenerative disorders, and skeletal issues VEGF, PDGF, PlGF, FGF, ANG, Notch, EphB, and PPAR γ 270 , 271 , 272 , 274 , 277 , 278 , 279 , 284 , 285 , 287 , 288 , 289 , 290 , ...…”

Section: Lessons To Learn From Cancer Complications and Comorbiditiesmentioning

confidence: 99%

Complications and comorbidities associated with antineoplastic chemotherapy: Rethinking drug design and delivery for anticancer therapy

Mao,

Wu,

Huang

et al. 2024

Acta Pharmaceutica Sinica B

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Let thy food be thy medicine….when possible

Witkamp

Norren

2018

European Journal of Pharmacology

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There is no evidence that Hippocrates, although being credited for it, ever literally stated 'let thy food be thy medicine and thy medicine be thy food'. However, yet in line with Hippocrates' philosophy, we are currently witnessing a reappraisal of the complementarity of nutrition and pharmacology. Recent studies not only underline the therapeutic potential of lifestyle interventions, but are also generating valuable insights in the complex and dynamic transition from health to disease. Next to this, nutritional biology can significantly contribute to the discovery of new molecular targets. It is clear that most of the current top-selling drugs used in chronic cardio-metabolic diseases modulate relatively late-stage complications, which generally indicate already longer existing homeostatic imbalances. Pharmacologists are increasingly aware that typical multifactorial disorders require subtle, multiple target pharmacological approaches, instead of the still often dominating 'one disease - one target - one drug' paradigm. This review discusses the recent developments in the pharma-nutrition interface and shows some relevant mechanisms, including receptors and other targets, and examples from clinical practice. The latter includes inflammatory diseases and progressive loss of muscle function. The examples also illustrate the potential of targeted combinations of medicines with nutrition and (or) other life-style interventions, to increase treatment efficacy and (or) reduce adverse effects. More attention to a potentially negative outcome of drug-food combinations is also required, as shown by the example of food-drug interactions. Together, the developments at the food-pharma interface underline the demand for intensified collaboration between the disciplines, in the clinic and in science.

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Treatment with high dose salicylates improves cardiometabolic parameters: Meta-analysis of randomized controlled trials

Cited by 4 publications

References 57 publications

Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms

Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms

Complications and comorbidities associated with antineoplastic chemotherapy: Rethinking drug design and delivery for anticancer therapy

Let thy food be thy medicine….when possible

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