Comparative study of coronary collaterals in diabetic and nondiabetic patients by angiography

Islam, M.Z.; Ali, Atahar; Na, Khan; Rahman, Abdur; Majumder, A.; Chowdhury, WA; Faruque, GM; Faruque, M; Jalaluddin, Muhammad

doi:10.3329/mmj.v15i2.38

Cited by 7 publications

(8 citation statements)

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“…However, both phases were more pronounced in diabetics compared with nondiabetic mice. Previous research reports indicate that diabetics have a reduced ability to grow collaterals (1,20). Our results raise the possibility that diabetics are actually capable of growing vessels, yet the extent of vessel rarefaction limits sustainable vessel growth.…”

Section: Discussioncontrasting

confidence: 52%

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Growth and regression of vasculature in healthy and diabetic mice after hindlimb ischemia

Landázuri

Joseph

Guldberg

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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The formation of vascular networks during embryogenesis and early stages of development encompasses complex and tightly regulated growth of blood vessels, followed by maturation of some vessels, and spatially controlled disconnection and pruning of others. The adult vasculature, while more quiescent, is also capable of adapting to changing physiological conditions by remodeling blood vessels. Numerous studies have focused on understanding key factors that drive vessel growth in the adult in response to ischemic injury. However, little is known about the extent of vessel rarefaction and its potential contribution to the final outcome of vascular recovery. We addressed this topic by characterizing the endogenous phases of vascular repair in a mouse model of hindlimb ischemia. We showed that this process is biphasic. It encompasses an initial rapid phase of vessel growth, followed by a later phase of vessel rarefaction. In healthy mice, this process resulted in partial recovery of perfusion and completely restored the ability of mice to run voluntarily. Given that the ability to revascularize can be compromised by a cardiovascular risk factor such as diabetes, we also examined vascular repair in diabetic mice. We found that paradoxically both the initial growth and subsequent regression of collateral vessels were more pronounced in the setting of diabetes and resulted in impaired recovery of perfusion and impaired functional status. In conclusion, our findings demonstrate that the formation of functional collateral vessels in the hindlimb requires vessel growth and subsequent vessel rarefaction. In the setting of diabetes, the physiological defect was not in the initial formation of vessels but rather in the inability to sustain newly formed vessels.

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Section: Discussioncontrasting

confidence: 52%

“…The adult vasculature, while more quiescent, is also capable of adapting to changing physiological conditions by remodeling blood vessels (9, 11, 29 -31). This ability can be compromised in the presence of cardiovascular risk factors such as diabetes (1,20).…”

mentioning

confidence: 99%

Growth and regression of vasculature in healthy and diabetic mice after hindlimb ischemia

Landázuri

Joseph

Guldberg

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Poor perfusion in diabetics has been attributed to their impaired ability to grow collateral vessels (2, 3) and our hypothesis was that these changes are due to AGE mediated signaling through RAGE. We induced diabetes with STZ and allowed the mice to remain diabetic for several weeks allowing for the formation of AGEs specifically CML (Figures 1 and 2).…”

Section: Discussionmentioning

confidence: 94%

“…This situation is further complicated by the fact that collateral vessel formation is markedly impaired in diabetics. (2, 3)…”

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confidence: 99%

The receptor for advanced glycation end products impairs collateral formation in both diabetic and non-diabetic mice

Hansen

Gupta

Joseph

et al. 2017

Laboratory Investigation

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Diabetics often have poor perfusion in their limbs as a result of peripheral artery disease and an impaired ability to generate collateral vessels. The receptor for advanced glycation end products (RAGE) is one protein that is thought to play a detrimental role in collateral development in diabetics due increased levels of advanced glycation end products (AGE), one of its ligands, in diabetes. Thus the aim of this study was to investigate the role of RAGE in both diabetic and non-diabetic settings in a model of collateral formation in mice. Streptozotocin was used to induce diabetes in both wild type and RAGE knockout mice. Increased levels of the AGE, Nε-(carboxymethyl) lysine (CML), were confirmed via an ELISA. A hindlimb ischemia model, in which the femoral artery is ligated, was used to drive collateral growth and reperfusion was assessed using laser Doppler perfusion imaging and histological analysis of vessels in the muscle. Both of these measurements showed impaired collateral growth in diabetic compared to wildtype mice as well as improved collateral growth in both diabetic and non-diabetic RAGE knockout mice when compared their wildtype counterparts. Distance on a freely accessed running wheel, used as a measure of perfusion recovery, showed that wildtype diabetic mice had functionally impaired recovery compared to their wildtype counterparts. Immunohistochemistry and immunoblotting showed that HMGB-1 (high mobility group box 1), another RAGE ligand, was increased in the ischemic leg compared to the non-ischemic leg in all mice. This increase in HMGB-1 may explain improvement in animals lacking RAGE and its subsequent signaling. In conclusion, this study shows that RAGE impairs collateral growth in a diabetic setting and also in a non-diabetic setting. This demonstrates the importance of RAGE and alternate RAGE ligands in the setting of collateral vessel growth.

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“…Titles and abstracts were screened for all papers produced by the literature search. Studies excluded from the primary analyses during title and abstract screening were reviews, 24 , 25 , 26 editorials, 27 animal or in vitro studies, 28 mechanistic studies (even if they used endpoints potentially related to clinical cancer, as epigenetic markers, telomere length, endocrine response), 29 , 30 , 31 , 32 papers on study protocols, 33 biostatistics methods papers, 34 , 35 epidemiological profiles and cohort descriptions, 36 , 37 risk/exposure assessments 38 and other studies where human cancer was not a primary outcome. 39 …”

Section: Methodsmentioning

confidence: 99%

Exposures to pesticides and risk of cancer: Evaluation of recent epidemiological evidence in humans and paths forward

Cavalier

Trasande

Porta

2022

Intl Journal of Cancer

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Knowledge of the role in cancer etiology of environmental exposures as pesticides is a prerequisite for primary prevention. We review 63 epidemiological studies on exposure to pesticides and cancer risk in humans published from 2017 to 2021, with emphasis on new findings, methodological approaches, and gaps in the existing literature. While much of the recent evidence suggests causal relationships between pesticide exposure and cancer, the strongest evidence exists for acute myeloid leukemia (AML) and colorectal cancer (CRC), diseases in which the observed associations were consistent across several studies, including high‐quality prospective studies and those using biomarkers for exposure assessment, with some observing dose‐response relationships. Though high‐quality studies have been published since the IARC monograph on organophosphate insecticides in 2017, there are still gaps in the literature on carcinogenic evidence in humans for a large number of pesticides. To further knowledge, we suggest leveraging new techniques and methods to increase sensitivity and precision of exposure assessment, incorporate multi‐omics data, and investigate more thoroughly exposure to chemical mixtures. There is also a strong need for better and larger population‐based cohort studies that include younger and nonoccupationally exposed individuals, particularly during developmental periods of susceptibility. Though the existing evidence has limitations, as always in science, there is sufficient evidence to implement policies and regulatory action that limit pesticide exposure in humans and, hence, further prevent a significant burden of cancers.

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Comparative study of coronary collaterals in diabetic and nondiabetic patients by angiography

Cited by 7 publications

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Growth and regression of vasculature in healthy and diabetic mice after hindlimb ischemia

Growth and regression of vasculature in healthy and diabetic mice after hindlimb ischemia

The receptor for advanced glycation end products impairs collateral formation in both diabetic and non-diabetic mice

Exposures to pesticides and risk of cancer: Evaluation of recent epidemiological evidence in humans and paths forward

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