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AbstractResource depletion and environmental pollution have seriously restricted the sustainable development of China's economy in recent years. How to transform the extensive growth mode to the intensive growth mode and realize the green development of economy is a great challenge for China. In this paper, we use the non‐radial and non‐angle Slack‐based Model (SBM) considering the undesired output, combined with the Malmquist–Luenberger productivity index, to measure regional green total factor productivity (GTFP). By constructing the green output density function, the theoretical model of the relationship between regional GTFP and industrial agglomeration is deduced, and the theoretical mechanism of the influence of industrial agglomeration on regional GTFP is analyzed. Based on panel data of 243 cities at the prefecture level in China from 2010 to 2019, this article employs the dynamic spatial panel model to empirically estimate the impact of industrial agglomeration on regional GTFP. The empirical results show that regional GTFP shows significant spatial autocorrelation and spatial clustering characteristics. The manufacturing agglomeration has significant negative impact on regional GTFP and produces negative spatial spillover effect on the surrounding regions, but does not produce congestion effect. The producer services agglomeration significantly improves regional GTFP and produces positive spatial spillover effect on the surrounding regions, and leads to congestion effect. The co‐agglomeration of producer services and manufacturing has significantly promoted the improvement of regional GTFP and produces positive spatial spillover effect on the surrounding regions. Finally, this article puts forward policy suggestions on how to promote regional GTFP and achieve green development from the perspective of industrial agglomeration.

Abstract
Vascular aging, a common pathogenesis of senile chronic diseases, significantly increases morbidity and mortality in older adults; its intricate cellular and molecular mechanisms necessitate further investigation. Lumican (LUM) and integrin α2β1(ITGα2β1) are profibrotic extracellular matrix proteins and vital cell regulatory receptors, respectively. However, their roles in vascular aging remain unclear. This study sought to elucidate the connection between LUM and vascular aging as well as the biological mechanism of LUM/ITGα2β1 in this process. Using an enzyme-linked immunosorbent assay, we discovered that plasma LUM was elevated in vascular aging individuals and was positively correlated with brachial-ankle pulse wave velocity. Additionally, immunohistochemical and western blot analyses confirmed LUM upregulation in arteries of older adults and aged mice, as well as in senescent vascular smooth cells (VSMCs). Wild-type and LUM semiknockout (Lum-/+) mice, along with primary VSMCs extracted from these mice, were exposed to angiotensin II (Ang II) to induce stress-induced senescence model. LUM semiknockout mitigated Ang Ⅱ-induced arteriosclerosis, hypertension, vascular aging and remodeling in mice. Both in vitro and in vivo studies revealed that LUM deficiency suppressed p53, p21, collagen 1 and collagen 3 upregulation and synthetic phenotype formation in VSMCs stimulated by Ang Ⅱ. Treating VSMCs with a ITGα2β1 antagonist reversed the aforementioned changes triggered by LUM proteins. Briefly, LUM functions as a potential marker and risk factor for vascular aging and promotes pathological changes by affecting ITGα2β1 in VSMCs. This study introduces a novel molecular target for the early diagnosis and treatment of vascular aging and age-related vascular diseases.